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1
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0024473604
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G1 events and regulation of cell proliferation
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Pardee AB. G1 events and regulation of cell proliferation. Science. 246:1989;603-608.
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(1989)
Science
, vol.246
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Pardee, A.B.1
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3
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0029033861
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The retinoblastoma protein and cell cycle control
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Weinberg RA. The retinoblastoma protein and cell cycle control. Cell. 81:1995;323-330.
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Cell
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Weinberg, R.A.1
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4
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0028886364
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Unrestricted cell cycling and cancer
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Strauss M, Lukas J, Bartek J. Unrestricted cell cycling and cancer. Nat Med. 1:1995;1245-1246.
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Nat Med
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Strauss, M.1
Lukas, J.2
Bartek, J.3
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5
-
-
0028911033
-
Activity of RNA polymerase I transcription factor UBF blocked by Rb gene product
-
of outstanding interest. This study provides the first evidence for the involvement of pRb in regulating the synthesis of ribosomal RNA. The ability of pRb to specifically inhibit the activity of RNA polymerase I is dependent on the pRb pocket domain, and is mediated via direct interaction with the pol I transcription factor UBF (upstream-binding factor).
-
Cavanaugh AH, Hempel WM, Taylor LJ, Rogalsky V, Todorov G, Rothblum LI. Activity of RNA polymerase I transcription factor UBF blocked by Rb gene product. of outstanding interest Nature. 374:1995;177-180 This study provides the first evidence for the involvement of pRb in regulating the synthesis of ribosomal RNA. The ability of pRb to specifically inhibit the activity of RNA polymerase I is dependent on the pRb pocket domain, and is mediated via direct interaction with the pol I transcription factor UBF (upstream-binding factor).
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(1995)
Nature
, vol.374
, pp. 177-180
-
-
Cavanaugh, A.H.1
Hempel, W.M.2
Taylor, L.J.3
Rogalsky, V.4
Todorov, G.5
Rothblum, L.I.6
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6
-
-
0029901988
-
Repression of RNA polymerase III transcription by the retinoblastoma protein
-
of outstanding interest. This report demonstrates the ability of pRb to repress transcription by pol III both in vivo and in vitro. Moreover, the pRb-mediated repression of pol III activity is shown to be alleviated by tumour-associated mutations within the pRb pocket domain, and via transforming oncoproteins that bind and inactivate pRb, implying that the restraint of protein biosynthesis may be important in the prevention of tumorigenesis.
-
White RJ, Trouche D, Martin K, Jackson SP, Kouzarides T. Repression of RNA polymerase III transcription by the retinoblastoma protein. of outstanding interest Nature. 382:1996;88-90 This report demonstrates the ability of pRb to repress transcription by pol III both in vivo and in vitro. Moreover, the pRb-mediated repression of pol III activity is shown to be alleviated by tumour-associated mutations within the pRb pocket domain, and via transforming oncoproteins that bind and inactivate pRb, implying that the restraint of protein biosynthesis may be important in the prevention of tumorigenesis.
-
(1996)
Nature
, vol.382
, pp. 88-90
-
-
White, R.J.1
Trouche, D.2
Martin, K.3
Jackson, S.P.4
Kouzarides, T.5
-
8
-
-
0029978325
-
E2F-4 switches from p130 to p107 and pRB in response to cell cycle reentry
-
of special interest. See annotation [7].
-
Moberg K, Starz MA, Lees JA. E2F-4 switches from p130 to p107 and pRB in response to cell cycle reentry. of special interest Mol Cell Biol. 16:1996;1436-1449 See annotation [7].
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(1996)
Mol Cell Biol
, vol.16
, pp. 1436-1449
-
-
Moberg, K.1
Starz, M.A.2
Lees, J.A.3
-
9
-
-
9444242683
-
Shared role of the pRB-related p130 and p107 proteins in limb development
-
of outstanding interest. This study provides in vivo evidence that two pRb-related pocket proteins, p130 and p107, share limited, tissue-restricted biological functions that could not be fully compensated for by pRb. Mice carrying homozygous mutations of either p107 or p130 developed normally, whereas animals concurrently nullizygous for both p130 and p107 exhibited impaired chondrocyte proliferation, resulting in defective bone development and neonatal lethality.
-
Cobrinik D, Lee M-H, Hannon G, Mulligan G, Bronson RT, Dyson N, Harlow E, Beach D, Weinberg RA, Jacks T. Shared role of the pRB-related p130 and p107 proteins in limb development. of outstanding interest Genes Dev. 10:1996;1633-1644 This study provides in vivo evidence that two pRb-related pocket proteins, p130 and p107, share limited, tissue-restricted biological functions that could not be fully compensated for by pRb. Mice carrying homozygous mutations of either p107 or p130 developed normally, whereas animals concurrently nullizygous for both p130 and p107 exhibited impaired chondrocyte proliferation, resulting in defective bone development and neonatal lethality.
-
(1996)
Genes Dev
, vol.10
, pp. 1633-1644
-
-
Cobrinik, D.1
Lee, M.-H.2
Hannon, G.3
Mulligan, G.4
Bronson, R.T.5
Dyson, N.6
Harlow, E.7
Beach, D.8
Weinberg, R.A.9
Jacks, T.10
-
10
-
-
0029736909
-
Targeted disruption of p107: Functional overlap between p107 and Rb
-
-/- animals, the authors of this study provide the first in vivo evidence that p107 and pRb have partially overlaping functions in some tissues of the developing and adult mouse.
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-/- animals, the authors of this study provide the first in vivo evidence that p107 and pRb have partially overlaping functions in some tissues of the developing and adult mouse.
-
(1996)
Genes Dev
, vol.10
, pp. 1621-1632
-
-
Lee, M.-H.1
Williams, B.O.2
Mulligan, G.3
Mukai, S.4
Bronson, R.T.5
Dyson, N.6
Harlow, E.7
Jacks, T.8
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11
-
-
0029863840
-
Altered cell cycle kinetics, gene expression, and G1 restriction point regulation in Rb-deficient fibroblasts
-
1 phase, and are more resistant to cycloheximide-mediated inhibition of proteosynthesis as compared with their wild-type littermates.
-
1 phase, and are more resistant to cycloheximide-mediated inhibition of proteosynthesis as compared with their wild-type littermates.
-
(1996)
Mol Cell Biol
, vol.16
, pp. 2402-2407
-
-
Herrera, R.E.1
Sah, V.P.2
Williams, B.O.3
Mäkelä, T.P.4
Weinberg, R.A.5
Jacks, T.6
-
12
-
-
0028925360
-
Cyclin D1 is dispensable for G1 control in retinoblastoma gene-deficient cells, independently of cdk4 activity
-
of outstanding interest. See annotation [11]. This study also shows that cyclin D - Cdk4 operates upstream of pRb.
-
Lukas J, Bartkova J, Rohde M, Strauss M, Bartek J. Cyclin D1 is dispensable for G1 control in retinoblastoma gene-deficient cells, independently of cdk4 activity. of outstanding interest Mol Cel Biol. 15:1995;2600-2611 See annotation [11]. This study also shows that cyclin D - Cdk4 operates upstream of pRb.
-
(1995)
Mol Cel Biol
, vol.15
, pp. 2600-2611
-
-
Lukas, J.1
Bartkova, J.2
Rohde, M.3
Strauss, M.4
Bartek, J.5
-
13
-
-
0029924241
-
Differential regulation of retinoblastoma protein function by specific Cdk phosphorylation sites
-
of special interest. Properties of pRb mutants lacking specific phosphorylation sites on pRb demonstrate that phosphorylation of Thr821/Thr826 regulates the association of human pRb with LXCXE (single-letter code for amino acids)-motif-containing proteins, whereas phosphorylation of Ser807/Ser811 of pRb is required to disrupt c-Abl binding.
-
Knudsen ES, Wang JYJ. Differential regulation of retinoblastoma protein function by specific Cdk phosphorylation sites. of special interest J Biol Chem. 271:1996;8313-8320 Properties of pRb mutants lacking specific phosphorylation sites on pRb demonstrate that phosphorylation of Thr821/Thr826 regulates the association of human pRb with LXCXE (single-letter code for amino acids)-motif-containing proteins, whereas phosphorylation of Ser807/Ser811 of pRb is required to disrupt c-Abl binding.
-
(1996)
J Biol Chem
, vol.271
, pp. 8313-8320
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-
Knudsen, E.S.1
Wang, J.Y.J.2
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14
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-
0028948160
-
Detection of a novel cell cycle-regulated kinase activity that associates with the amino terminus of the retinoblastoma protein in G2/M phases
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Sterner JM, Yosihiko M, Goo Kim H, Kennett SB, Templeton DJ, Horowitz JM. Detection of a novel cell cycle-regulated kinase activity that associates with the amino terminus of the retinoblastoma protein in G2/M phases. J Biol Chem. 270:1995;9281-9288.
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(1995)
J Biol Chem
, vol.270
, pp. 9281-9288
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-
Sterner, J.M.1
Yosihiko, M.2
Goo Kim, H.3
Kennett, S.B.4
Templeton, D.J.5
Horowitz, J.M.6
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16
-
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0028988585
-
Inhibitors of mammalian G1 cyclin-dependent kinases
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Sherr CJ, Roberts JM. Inhibitors of mammalian G1 cyclin-dependent kinases. Genes Dev. 9:1995;1149-1163.
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(1995)
Genes Dev
, vol.9
, pp. 1149-1163
-
-
Sherr, C.J.1
Roberts, J.M.2
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17
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0029009876
-
Different roles for cyclins D1 and E in regulation of the G1-to-S transition
-
1→S-phase transition by modulating a different, unknown substrate.
-
1→S-phase transition by modulating a different, unknown substrate.
-
(1995)
Mol Cell Biol
, vol.15
, pp. 3463-3469
-
-
Resnitzky, D.1
Reed, S.I.2
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18
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0029054399
-
REtinoblastoma-protein-dependent cell-cycle inhibition by the tumour supressor p16
-
of outstanding interest. This study, together with [19,20], showed that the growth-restraining potential of p16 requires the presence of functional pRb. It was also demonstrated that melanoma-associated point mutations in p16 represent true loss-of-function alleles, supporting the notion of p16 as a bona fide tumour suppressor.
-
Lukas J, Parry D, Aagaard L, Mann DJ, Bartkova J, Strauss M, Peters G, Bartek J. REtinoblastoma-protein-dependent cell-cycle inhibition by the tumour supressor p16. of outstanding interest Nature. 375:1995;503-506 This study, together with [19,20], showed that the growth-restraining potential of p16 requires the presence of functional pRb. It was also demonstrated that melanoma-associated point mutations in p16 represent true loss-of-function alleles, supporting the notion of p16 as a bona fide tumour suppressor.
-
(1995)
Nature
, vol.375
, pp. 503-506
-
-
Lukas, J.1
Parry, D.2
Aagaard, L.3
Mann, D.J.4
Bartkova, J.5
Strauss, M.6
Peters, G.7
Bartek, J.8
-
19
-
-
0029052951
-
Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition
-
of outstanding interest. See annotation [18].
-
Koh J, Enders GH, Dynlacht BD, Harlow E. Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition. of outstanding interest Nature. 375:1995;506-510 See annotation [18].
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(1995)
Nature
, vol.375
, pp. 506-510
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-
Koh, J.1
Enders, G.H.2
Dynlacht, B.D.3
Harlow, E.4
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22
-
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0029024332
-
Overexpression of human cyclin A advances entry into S phase
-
Rosenberg AR, Zindy F, Le Deist R, Mouly H, Métézeau P, Bréchot C, Lamas E. Overexpression of human cyclin A advances entry into S phase. Oncogene. 10:1995;1501-1509.
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(1995)
Oncogene
, vol.10
, pp. 1501-1509
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-
Rosenberg, A.R.1
Zindy, F.2
Le Deist, R.3
Mouly, H.4
Métézeau, P.5
Bréchot, C.6
Lamas, E.7
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23
-
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0028909645
-
Human cyclin E, a nuclear protein essential for the G1-to-S phase transition
-
1-phase progression in pRb-negative, as well as pRb-positive, cells.
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1-phase progression in pRb-negative, as well as pRb-positive, cells.
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(1995)
Mol Cell Biol
, vol.15
, pp. 2612-2624
-
-
Ohtsubo, M.1
Theodoras, A.M.2
Schumacher, J.3
Roberts, J.M.4
Pagano, M.5
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24
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0029038504
-
Cyclin-dependent kinases and pRb: Regulators of the proliferation-differentiation switch
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Kranenburg O, Van der Eb AJ, Zantema A. Cyclin-dependent kinases and pRb: regulators of the proliferation-differentiation switch. FEBS Letts. 367:1995;103-106.
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(1995)
FEBS Letts
, vol.367
, pp. 103-106
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-
Kranenburg, O.1
Van Der Eb, A.J.2
Zantema, A.3
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25
-
-
0030008768
-
Expression of dominant-negative mutant DP-1 blocks cell cycle progression in G1
-
of special interest. Describes the most direct demonstration so far of a requirement for active E2F complexes in mammalian cell progression.
-
Wu C-L, Classon M, Dyson N, Harlow E. Expression of dominant-negative mutant DP-1 blocks cell cycle progression in G1. of special interest Mol Cell Biol. 16:1996;3698-3706 Describes the most direct demonstration so far of a requirement for active E2F complexes in mammalian cell progression.
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(1996)
Mol Cell Biol
, vol.16
, pp. 3698-3706
-
-
Wu, C.-L.1
Classon, M.2
Dyson, N.3
Harlow, E.4
-
27
-
-
0029888359
-
Tumor induction and tissue atrophy in mice lacking E2F-1
-
of outstanding interest. This study and [28] address the function of E2F1 and pRb - E2F1 complexes in vivo by generating mice that are homozygous for a nonfunctional E2F1 allele. Surprisingly, E2F1-deficient animals are viable and fertile but develop a broad spectrum of tumors. Therefore, E2F1 may serve as either a proto-oncoprotein or as a tumour suppressor, depending on cellular context.
-
Yamasaki L, Jacks T, Bronson R, Goillot E, Harlow E, Dyson NJ. Tumor induction and tissue atrophy in mice lacking E2F-1. of outstanding interest Cell. 85:1996;537-548 This study and [28] address the function of E2F1 and pRb - E2F1 complexes in vivo by generating mice that are homozygous for a nonfunctional E2F1 allele. Surprisingly, E2F1-deficient animals are viable and fertile but develop a broad spectrum of tumors. Therefore, E2F1 may serve as either a proto-oncoprotein or as a tumour suppressor, depending on cellular context.
-
(1996)
Cell
, vol.85
, pp. 537-548
-
-
Yamasaki, L.1
Jacks, T.2
Bronson, R.3
Goillot, E.4
Harlow, E.5
Dyson, N.J.6
-
28
-
-
0029949784
-
E2F-1 functions in mice to promote apoptosis and suppress proliferation
-
of outstanding interest. See annotation [27].
-
Field SJ, Tsai F-Y, Kuo F, Zubiaga AM, Kaelin WG, Livingston DM, Orkin SH, Greenberg ME. E2F-1 functions in mice to promote apoptosis and suppress proliferation. of outstanding interest Cell. 85:1996;549-561 See annotation [27].
-
(1996)
Cell
, vol.85
, pp. 549-561
-
-
Field, S.J.1
Tsai, F.-Y.2
Kuo, F.3
Zubiaga, A.M.4
Kaelin, W.G.5
Livingston, D.M.6
Orkin, S.H.7
Greenberg, M.E.8
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29
-
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0028826881
-
E2F-1 accumulation bypasses a G1 arrest resulting from the inhibition of G1 cyclin-dependent kinase activity
-
DeGregori J, Leone G, Ohtani K, Miron A, Nevins JR. E2F-1 accumulation bypasses a G1 arrest resulting from the inhibition of G1 cyclin-dependent kinase activity. Genes Dev. 9:1995;2873-2887.
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(1995)
Genes Dev
, vol.9
, pp. 2873-2887
-
-
DeGregori, J.1
Leone, G.2
Ohtani, K.3
Miron, A.4
Nevins, J.R.5
-
31
-
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0029926060
-
Differential effects of cdk2 and cdk3 on the control of pRb and E2F function during G1 exit
-
of outstanding interest. Active E2F, released from pRb or the related pocket proteins, failed to induce S phase in the presence of dominant-negative mutants of Cdk2 and Cdk3. Additional data support a pRb-independent contribution of Cdk3 to activation of E2F.
-
Hofmann F, Livingston DM. Differential effects of cdk2 and cdk3 on the control of pRb and E2F function during G1 exit. of outstanding interest Genes Dev. 10:1996;851-861 Active E2F, released from pRb or the related pocket proteins, failed to induce S phase in the presence of dominant-negative mutants of Cdk2 and Cdk3. Additional data support a pRb-independent contribution of Cdk3 to activation of E2F.
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(1996)
Genes Dev
, vol.10
, pp. 851-861
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-
Hofmann, F.1
Livingston, D.M.2
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32
-
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0029942908
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Cell cycle regulation of the murine cyclin E gene depends on an E2F binding site in the promoter
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Botz J, Zerfass-Thome K, Spitkovski D, Delius H, Vogt B, Eilers M, Hatzigeorgiou A, Jansen-Dürr P. Cell cycle regulation of the murine cyclin E gene depends on an E2F binding site in the promoter. Mol Cell Biol. 16:1996;3401-3409.
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(1996)
Mol Cell Biol
, vol.16
, pp. 3401-3409
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-
Botz, J.1
Zerfass-Thome, K.2
Spitkovski, D.3
Delius, H.4
Vogt, B.5
Eilers, M.6
Hatzigeorgiou, A.7
Jansen-Dürr, P.8
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33
-
-
0029986337
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Regulation of cyclin E transcription by E2Fs and retinoblastoma protein
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Geng Y, Ng Eaton E, Picón M, Roberts JM, Lundberg AS, Gifford A, Sardet C, Weinberg RA. Regulation of cyclin E transcription by E2Fs and retinoblastoma protein. Oncongene. 12:1996;1173-1180.
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(1996)
Oncongene
, vol.12
, pp. 1173-1180
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Geng, Y.1
Ng Eaton, E.2
Picón, M.3
Roberts, J.M.4
Lundberg, A.S.5
Gifford, A.6
Sardet, C.7
Weinberg, R.A.8
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34
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0029583648
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Regulation of the cyclin E gene by transcription factor E2F1
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Ohtani K, DeGregori J, Nevins JR. Regulation of the cyclin E gene by transcription factor E2F1. Proc Natl Acad Sci USA. 92:1995;12146-12150.
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(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 12146-12150
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Ohtani, K.1
DeGregori, J.2
Nevins, J.R.3
-
35
-
-
0028892480
-
Cell cycle regulation of the cyclin A gene promoter is mediated by a variant E2F site
-
Schulze A, Zerfass K, Spitkovsky D, Middendorp S, Bergès J, Helin K, Jansen-Dürr P, Henglein B. Cell cycle regulation of the cyclin A gene promoter is mediated by a variant E2F site. Proc Natl Acad Sci USA. 92:1995;11264-11268.
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Proc Natl Acad Sci USA
, vol.92
, pp. 11264-11268
-
-
Schulze, A.1
Zerfass, K.2
Spitkovsky, D.3
Middendorp, S.4
Bergès, J.5
Helin, K.6
Jansen-Dürr, P.7
Henglein, B.8
-
36
-
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0028980858
-
Developmental control of the G1 to S transition in Drosophila: Cyclin E is a limiting downstream target of E2F
-
1 phase can bypass E2F and induce DNA replication.
-
1 phase can bypass E2F and induce DNA replication.
-
(1995)
Genes Dev
, vol.9
, pp. 1456-1468
-
-
Duronio, R.J.1
O'Farrell, P.H.2
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38
-
-
0029670840
-
CDKN2 expression and its implications for cell immortalization and senescence
-
of special interest. Overexpression of p16 in pRb-negative cells is caused by at least two factors: a loss of repression by pRb, and a gradual accumulation of p16 as the population doubles repeatedly.
-
CDKN2 expression and its implications for cell immortalization and senescence. of special interest Mol Cell Biol. 16:1996;859-867 Overexpression of p16 in pRb-negative cells is caused by at least two factors: a loss of repression by pRb, and a gradual accumulation of p16 as the population doubles repeatedly.
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(1996)
Mol Cell Biol
, vol.16
, pp. 859-867
-
-
Hara, E.1
Smith, R.2
Parry, D.3
Tahara, H.4
Stone, S.5
Peters, G.6
-
40
-
-
0028978183
-
Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
-
1 phase in response to DNA damage, and grew to aberrantly higher saturation densities.
-
1 phase in response to DNA damage, and grew to aberrantly higher saturation densities.
-
(1995)
Cell
, vol.82
, pp. 675-684
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-
Deng, C.1
Zhang, P.2
Harper, J.W.3
Elledge, S.J.4
Leder, P.5
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41
-
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0029097759
-
Radiation-induced cell cycle arrest compromised by p21 deficiency
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Brugarolas J, Chandrasekaran C, Gordon JI, Beach D, Jacks T, Hannon GJ. Radiation-induced cell cycle arrest compromised by p21 deficiency. Nature. 377:1995;552-557.
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(1995)
Nature
, vol.377
, pp. 552-557
-
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Brugarolas, J.1
Chandrasekaran, C.2
Gordon, J.I.3
Beach, D.4
Jacks, T.5
Hannon, G.J.6
-
42
-
-
0029664461
-
Kip1 for restriction point control of the fibroblast cell cycle
-
Kip1 by antisense DNA prevents cell cycle arrest in response to mitogen depletion. Both studies suggest p27 as an essential molecular component linking mitogenic signalling to R.
-
Kip1 by antisense DNA prevents cell cycle arrest in response to mitogen depletion. Both studies suggest p27 as an essential molecular component linking mitogenic signalling to R.
-
(1996)
Science
, vol.272
, pp. 877-880
-
-
Coats, S.1
Flanagan, W.M.2
Nourse, J.3
Roberts, J.M.4
-
43
-
-
0029666482
-
Abrogation of p27Kip1 by cDNA antisense suppresses quiescence (GO state) in fibroblasts
-
of outstanding interest. See annotation [42].
-
Rivard N, L'Allemain G, Bartek J, Pouysségur J. Abrogation of p27Kip1 by cDNA antisense suppresses quiescence (GO state) in fibroblasts. of outstanding interest J Biol Chem. 271:1996;18337-18341 See annotation [42].
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(1996)
J Biol Chem
, vol.271
, pp. 18337-18341
-
-
Rivard, N.1
L'Allemain, G.2
Bartek, J.3
Pouysségur, J.4
-
44
-
-
15844384256
-
A syndrome of multiorgan hyperplasia with features of gigantism, tumorigenesis, and female sterility in p27Kip1-deficient mice
-
-/- animals were enlarged and contained more and smaller cells compared with normal littermates. Moreover, T cells lacking p27 showed enhanced IL-2 responsiveness. The authors concluded that p27 deficiency may cause a cell-autonomous defect, resulting in enhanced proliferation in response to mitogens. See also [45,46].
-
-/- animals were enlarged and contained more and smaller cells compared with normal littermates. Moreover, T cells lacking p27 showed enhanced IL-2 responsiveness. The authors concluded that p27 deficiency may cause a cell-autonomous defect, resulting in enhanced proliferation in response to mitogens. See also [45,46].
-
(1996)
Cell
, vol.85
, pp. 733-744
-
-
Fero, M.L.1
Rivkin, M.2
Tasch, M.3
Porter, P.4
Carow, C.E.5
Firpo, E.6
Polyak, K.7
Tsai, L.-H.8
Broudy, V.9
Perlmutter, R.M.10
-
45
-
-
15844415946
-
Enhanced growth of mice lacking the cyclin-dependent kinase inhibitor function of p27Kip1
-
of outstanding interest. See annotation [44].
-
Kiyokawa H, Kineman RD, Manova-Todorova KO, Soares VC, Hoffman ES, Ono M, Khanam D, Hayday AC, Frohman LA, Koff A. Enhanced growth of mice lacking the cyclin-dependent kinase inhibitor function of p27Kip1. of outstanding interest Cell. 85:1996;721-732 See annotation [44].
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(1996)
Cell
, vol.85
, pp. 721-732
-
-
Kiyokawa, H.1
Kineman, R.D.2
Manova-Todorova, K.O.3
Soares, V.C.4
Hoffman, E.S.5
Ono, M.6
Khanam, D.7
Hayday, A.C.8
Frohman, L.A.9
Koff, A.10
-
46
-
-
0030010591
-
Mice lacking p27Kip1 display increased body size, multiple organ hyperplasia, retinal dysplasia, and pituitary tumors
-
1 phase in response to transforming growth factor β, rapamycin or contact inhibition.
-
1 phase in response to transforming growth factor β, rapamycin or contact inhibition.
-
(1996)
Cell
, vol.85
, pp. 707-720
-
-
Nakayama, K.1
Ishida, N.2
Shirane, M.3
Inomata, A.4
Inoue, T.5
Shishido, N.6
Horii, I.7
Loh, D.Y.8
Nakayama, K.-I.9
-
47
-
-
0029024015
-
Role of the ubiquitin - Proteasome pathway in regulating amounts of the cyclin-dependent kinase inhibitor p27
-
of outstanding interest. This paper provides the first evidence that p27 levels in mammalian cells are regulated by the ubiquitin - proteasome pathway.
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Pagano M, Tam SW, Theodoras AM, Beer-Romero P, Del Sal G, Chau V, Yew PR, Draetta GF, Rolfe M. Role of the ubiquitin - proteasome pathway in regulating amounts of the cyclin-dependent kinase inhibitor p27. of outstanding interest Science. 269:1995;682-685 This paper provides the first evidence that p27 levels in mammalian cells are regulated by the ubiquitin - proteasome pathway.
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(1995)
Science
, vol.269
, pp. 682-685
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Pagano, M.1
Tam, S.W.2
Theodoras, A.M.3
Beer-Romero, P.4
Del Sal, G.5
Chau, V.6
Yew, P.R.7
Draetta, G.F.8
Rolfe, M.9
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48
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0029670477
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Translational control of p27Kip1 accumulation during the cell cycle
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of special interest. This study revealed an additional mechanism of control of p27 protein levels, namely regulation of translation.
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Hengst L, Reed SI. Translational control of p27Kip1 accumulation during the cell cycle. of special interest Science. 271:1996;1861-1864 This study revealed an additional mechanism of control of p27 protein levels, namely regulation of translation.
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(1996)
Science
, vol.271
, pp. 1861-1864
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-
Hengst, L.1
Reed, S.I.2
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49
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0029153609
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Kip/cip and Ink4 cdk inhibitors cooperate to induce cell cycle arrest in response to TGF-β
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INK4B, liberates the p27 CKI from Cdk4/6, and results in redistribution of p72 to Cdk2.
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INK4B, liberates the p27 CKI from Cdk4/6, and results in redistribution of p72 to Cdk2.
-
(1995)
Genes Dev
, vol.9
, pp. 1831-1845
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-
Reynisdottir, I.1
Polyak, K.2
Iavarone, A.3
Massague, J.4
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50
-
-
0029050533
-
Deficiency of retinoblastoma protein leads to inappropriate S-phase entry, activation of E2F-responsive genes, and apoptosis
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of special interest. The authors demonstrate that mouse embryonic fibroblasts lacking both Rb alleles could enter S phase in the presence of the dihydrofolate reductase inhibitor methotrexate.
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Almasan A, Yin Y, Kelly RE, Lee EY-HP, Bradley A, Li W, Bertino JR, Wahl GM. Deficiency of retinoblastoma protein leads to inappropriate S-phase entry, activation of E2F-responsive genes, and apoptosis. of special interest Proc Natl Acad Sci USA. 92:1995;5436-5440 The authors demonstrate that mouse embryonic fibroblasts lacking both Rb alleles could enter S phase in the presence of the dihydrofolate reductase inhibitor methotrexate.
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(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 5436-5440
-
-
Almasan, A.1
Yin, Y.2
Kelly, R.E.3
Lee, E.Y.-H.P.4
Bradley, A.5
Li, W.6
Bertino, J.R.7
Wahl, G.M.8
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51
-
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0028990221
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Exit from GO and entry into the cell cycle of cells expressing p21Sdi1 antisense RNA
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Nakanishi M, Adami GR, Robetorye RS, Noda A, Venable SF, Dimitrov D, Pereira-Smith O, Smith JR. Exit from GO and entry into the cell cycle of cells expressing p21Sdi1 antisense RNA. Proc Natl Acad Sci USA. 92:1995;4352-4356.
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(1995)
Proc Natl Acad Sci USA
, vol.92
, pp. 4352-4356
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-
Nakanishi, M.1
Adami, G.R.2
Robetorye, R.S.3
Noda, A.4
Venable, S.F.5
Dimitrov, D.6
Pereira-Smith, O.7
Smith, J.R.8
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52
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0029111934
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Cyclin D1 provides a link between development and oncogenesis in the retina and breast
-
of outstanding interest. See annotation [53].
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Sicinski P, Liu Donaher J, Parker SB, Li T, Fazeli A, Gardner H, Haslam SZ, Bronson RT, Elledge SJ, Weinberg RA. Cyclin D1 provides a link between development and oncogenesis in the retina and breast. of outstanding interest Cell. 82:1995;621-630 See annotation [53].
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(1995)
Cell
, vol.82
, pp. 621-630
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-
Sicinski, P.1
Liu Donaher, J.2
Parker, S.B.3
Li, T.4
Fazeli, A.5
Gardner, H.6
Haslam, S.Z.7
Bronson, R.T.8
Elledge, S.J.9
Weinberg, R.A.10
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53
-
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0028889751
-
Mice lacking cyclin D1 are small and show defects in eye and mammary gland development
-
of outstanding interest. This paper and [52] report the phenotypic changes in transgenic mice lacking cyclin D1. Cyclin D1 deficient animals showed reduced body size and hypoproliferative symptoms such as retinal dysplasia, failure of the breast epithelium to undergo proliferative changes associated with pregnancy, and defects in jaw development.
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Fantl V, Stamp G, Andrews A, Rosewell I, Dickson C. Mice lacking cyclin D1 are small and show defects in eye and mammary gland development. of outstanding interest Genes Dev. 9:1995;2364-2372 This paper and [52] report the phenotypic changes in transgenic mice lacking cyclin D1. Cyclin D1 deficient animals showed reduced body size and hypoproliferative symptoms such as retinal dysplasia, failure of the breast epithelium to undergo proliferative changes associated with pregnancy, and defects in jaw development.
-
(1995)
Genes Dev
, vol.9
, pp. 2364-2372
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Fantl, V.1
Stamp, G.2
Andrews, A.3
Rosewell, I.4
Dickson, C.5
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54
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0029821233
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Expression of cyclin D1 in epithelial tissues of transgenic mice results in epidermal hyperproliferation and severe thymic hyperplasia
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Robles AI, Larcher F, Whalin RB, Murillas R, Richie E, Gimenez-Conti IB, Jorcano JL, Conti CJ. Expression of cyclin D1 in epithelial tissues of transgenic mice results in epidermal hyperproliferation and severe thymic hyperplasia. Proc Natl Acad Sci USA. 93:1996;7634-7638.
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(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 7634-7638
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-
Robles, A.I.1
Larcher, F.2
Whalin, R.B.3
Murillas, R.4
Richie, E.5
Gimenez-Conti, I.B.6
Jorcano, J.L.7
Conti, C.J.8
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56
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0029017456
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Ras transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells
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Liu J-J, Chao J-R, Jiang M-C, Ng S-Y, Jong-Young Yen J, Yang-Yen H-F. Ras transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells. Mol Cell Biol. 15:1995;3654-3663.
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(1995)
Mol Cell Biol
, vol.15
, pp. 3654-3663
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-
Liu, J.-J.1
Chao, J.-R.2
Jiang, M.-C.3
Ng, S.-Y.4
Jong-Young Yen, J.5
Yang-Yen, H.-F.6
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58
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85047678184
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Thyrotropin induces G1 cyclin expression and accelerates G1 phase after insulin-like growth factor I stimulation in FRTL-5 cells
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Yamamoto K, Hirai A, Ban T, Saito J, Tahara K, Terano T, Tamura Y, Saito Y, Kitagawa M. Thyrotropin induces G1 cyclin expression and accelerates G1 phase after insulin-like growth factor I stimulation in FRTL-5 cells. Endocrinology. 137:1996;2036-2042.
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(1996)
Endocrinology
, vol.137
, pp. 2036-2042
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-
Yamamoto, K.1
Hirai, A.2
Ban, T.3
Saito, J.4
Tahara, K.5
Terano, T.6
Tamura, Y.7
Saito, Y.8
Kitagawa, M.9
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59
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0029910364
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Convergence of mitogenic signalling cascades from diverse classes of receptors on the cyclin D/cdk-pRb-controlled G1 checkpoint
-
This study provides direct evidence that mitogenic stimuli from distinct signalling cascades (i.e. those activated by growth factors via tyrosine kinase receptors, by estradiol via estrogen receptors, and by cAMP-elevating agents via G protein coupled thyrotropin receptors) all converge and strictly require cyclin D - Cdk activity to promote S-phase onset. of special interest
-
Lukas J, Bartkova J, Bartek J. Convergence of mitogenic signalling cascades from diverse classes of receptors on the cyclin D/cdk-pRb-controlled G1 checkpoint. of special interest Mol Cell Biol. 1996; This study provides direct evidence that mitogenic stimuli from distinct signalling cascades (i.e. those activated by growth factors via tyrosine kinase receptors, by estradiol via estrogen receptors, and by cAMP-elevating agents via G protein coupled thyrotropin receptors) all converge and strictly require cyclin D - Cdk activity to promote S-phase onset.
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(1996)
Mol Cell Biol
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Lukas, J.1
Bartkova, J.2
Bartek, J.3
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60
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0029876639
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Adhesion-dependent cell cycle progression linked to the expression of cyclin D1, activation of cyclin E - Cdk2, and phosphorylation of the retinoblastoma protein
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Zhu X, Ohtsubo M, Böhmer RM, Roberts JM, Assoian RK. Adhesion-dependent cell cycle progression linked to the expression of cyclin D1, activation of cyclin E - cdk2, and phosphorylation of the retinoblastoma protein. J Cell Biol. 133:1996;391-403.
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(1996)
J Cell Biol
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, pp. 391-403
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Zhu, X.1
Ohtsubo, M.2
Böhmer, R.M.3
Roberts, J.M.4
Assoian, R.K.5
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61
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0030028947
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Cytoskeletal integrity is required throughout the mitogen stimulation phase of the cell cycle and mediates the anchorage-dependent expression of cyclin D1
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Böhmer RM, Scharf E, Assoian RK. Cytoskeletal integrity is required throughout the mitogen stimulation phase of the cell cycle and mediates the anchorage-dependent expression of cyclin D1. Mol Biol Cell. 7:1996;101-111.
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(1996)
Mol Biol Cell
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, pp. 101-111
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Böhmer, R.M.1
Scharf, E.2
Assoian, R.K.3
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62
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0029145975
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Redistribution of the CDK inhibitor p27 between different cyclin CDK complexes in the mouse fibroblast cell cycle and in cells arrested with lovastatin or ultraviolet irradiation
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Poon RYC, Toyoshima H, Hunter T. Redistribution of the CDK inhibitor p27 between different cyclin CDK complexes in the mouse fibroblast cell cycle and in cells arrested with lovastatin or ultraviolet irradiation. Mol Biol Cell. 6:1995;1197-1213.
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(1995)
Mol Biol Cell
, vol.6
, pp. 1197-1213
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Poon, R.Y.C.1
Toyoshima, H.2
Hunter, T.3
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63
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9044232147
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Formation of p27 - CDK complexes during the human mitotic cell cycle
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Soos TJ, Kiyokawa H, Shi Yan J, Rubin MS, Giordano A, DeBlasio A, Bottega S, Wong B, Mendelsohn J, Koff A. Formation of p27 - CDK complexes during the human mitotic cell cycle. Cell Growth Diff. 7:1996;135-146.
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(1996)
Cell Growth Diff
, vol.7
, pp. 135-146
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Soos, T.J.1
Kiyokawa, H.2
Shi Yan, J.3
Rubin, M.S.4
Giordano, A.5
DeBlasio, A.6
Bottega, S.7
Wong, B.8
Mendelsohn, J.9
Koff, A.10
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64
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0029941446
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Inhibition of p53-mediated growth arrest by overexpression of cyclin-dependent kinases
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Latham KM, Eastman SW, Wong A, Hinds PW. Inhibition of p53-mediated growth arrest by overexpression of cyclin-dependent kinases. Mol Cell Biol. 16:1996;4445-4455.
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(1996)
Mol Cell Biol
, vol.16
, pp. 4445-4455
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Latham, K.M.1
Eastman, S.W.2
Wong, A.3
Hinds, P.W.4
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65
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0029921317
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Genetic alterations of cyclins, cyclin-dependent kinases, and cdk inhibitors in human cancer
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Hall M, Peters G. Genetic alterations of cyclins, cyclin-dependent kinases, and cdk inhibitors in human cancer. Adv Cancer Res. 68:1996;67-108.
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(1996)
Adv Cancer Res
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, pp. 67-108
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Hall, M.1
Peters, G.2
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66
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0028978274
-
INK4a-insensitive cdk4 mutant targeted by cytolytic T lymphocytes in a human melanoma
-
of special interest. A point missense mutant Cdk4 found in human melanomas is deficient in its ability to associate with p16, indicating a novel mechanism used by tumour cells to escape from growth-restraining regulation by p16. The results also implicate mutant Cdk4 as a tumour-specific T-cell antigen.
-
INK4a-insensitive cdk4 mutant targeted by cytolytic T lymphocytes in a human melanoma. of special interest Science. 269:1995;1281-1284 A point missense mutant Cdk4 found in human melanomas is deficient in its ability to associate with p16, indicating a novel mechanism used by tumour cells to escape from growth-restraining regulation by p16. The results also implicate mutant Cdk4 as a tumour-specific T-cell antigen.
-
(1995)
Science
, vol.269
, pp. 1281-1284
-
-
Wölfel, T.1
Hauer, M.2
Schneider, J.3
Serrano, M.4
Wölfel, C.5
Klehmann-Hieb, E.6
De Plaen, E.7
Hankeln, T.8
Meyer Zum Büschenfelde, K.-H.9
Beach, D.10
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67
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0030467624
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The 'p16 - Cyclin D/Cdk4 - PRb' pathway as a functional unit frequently altered in melanoma pathogenesis
-
in press
-
Bartkova J, Lukas J, Guldberg P, Alsner J, Kirkin AF, Zeuthen J, Bartek J. The 'p16 - cyclin D/Cdk4 - pRb' pathway as a functional unit frequently altered in melanoma pathogenesis. Cancer Res. 1996;. in press.
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(1996)
Cancer Res
-
-
Bartkova, J.1
Lukas, J.2
Guldberg, P.3
Alsner, J.4
Kirkin, A.F.5
Zeuthen, J.6
Bartek, J.7
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68
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0029011539
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5′ CpG island methylation is associated with transcriptional silencing of the tumour suppressor p16/CDKN2/MTS1 in human cancers
-
of special interest. Provides the first demonstration that hypermethylation of the 5′ CpG islands of the p16 gene may represent an additional, and relatively frequent, mechanism of inactivating this tumour suppressor gene in human cancers.
-
Merlo A, Herman JG, Mao L, Lee DJ, Gabrielson E, Burger PC, Baylin SB, Sidransky D. 5′ CpG island methylation is associated with transcriptional silencing of the tumour suppressor p16/CDKN2/MTS1 in human cancers. of special interest Nat Med. 1:1995;686-692 Provides the first demonstration that hypermethylation of the 5′ CpG islands of the p16 gene may represent an additional, and relatively frequent, mechanism of inactivating this tumour suppressor gene in human cancers.
-
(1995)
Nat Med
, vol.1
, pp. 686-692
-
-
Merlo, A.1
Herman, J.G.2
Mao, L.3
Lee, D.J.4
Gabrielson, E.5
Burger, P.C.6
Baylin, S.B.7
Sidransky, D.8
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69
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0029808234
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Enhanced protein stability: A novel mechanism of D-type cyclin overabundance identified in human sarcoma cells
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Welcker M, Lukas J, Strauss M, Bartek J. Enhanced protein stability: a novel mechanism of D-type cyclin overabundance identified in human sarcoma cells. Oncogene. 13:1996;419-425.
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(1996)
Oncogene
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, pp. 419-425
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Welcker, M.1
Lukas, J.2
Strauss, M.3
Bartek, J.4
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70
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0028967830
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Cyclin D1 oncoprotein aberrantly accumulates in malignancies of diverse histogenesis
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Bartkova J, Lukas J, Strauss M, Bartek J. Cyclin D1 oncoprotein aberrantly accumulates in malignancies of diverse histogenesis. Oncogene. 10:1995;775-778.
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Oncogene
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, pp. 775-778
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Bartkova, J.1
Lukas, J.2
Strauss, M.3
Bartek, J.4
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