-
1
-
-
0027215414
-
Platelet-derived growth factor. Structure, function and implications in normal and malignant cell growth
-
(1993)
Acta Oncol
, vol.32
, pp. 101-105
-
-
Westermark1
Heldin2
-
3
-
-
0026810462
-
The emerging neuropoietic cytokine family: first CDF/LIF, CNTF and IL-6; next ONC, MGF, GCSF?
-
(1992)
Curr Opin Neurobiol
, vol.2
, pp. 94-97
-
-
Patterson1
-
5
-
-
0027285510
-
GDNF: a glial cell line-derived neurotrophic factor for midbrain dopaminergic neurons
-
of special interest, This paper describes the isolation and cloning of a new neurotrophic factor, glial-derived neurotrophic factor. Although initially thought to be specific for dopaminergic neurons, recent studies [18] indicate that it may have a broad spectrum of action.
-
(1993)
Science
, vol.260
, pp. 1130-1132
-
-
Lin1
Doherty2
Lile3
Bektesh4
Collins5
-
7
-
-
0028073706
-
Neurotrophic factors: an evolutionary perspective
-
(1994)
J Neurobiol
, vol.25
, pp. 1329-1333
-
-
Barde1
-
9
-
-
0026730310
-
Neurotrophin receptors: a window into neuronal differentiation
-
(1992)
Neuron
, vol.9
, pp. 583-593
-
-
Chao1
-
10
-
-
0028090302
-
The Trk family of neurotrophin receptors
-
(1994)
J Neurobiol
, vol.25
, pp. 1386-1403
-
-
Barbacid1
-
11
-
-
0027942459
-
The p75 neurotrophin receptor
-
(1994)
J Neurobiol
, vol.25
, pp. 1373-1385
-
-
Chao1
-
12
-
-
0027328343
-
The alphas, betas, and kinases of cytokine receptor complexes
-
(1993)
Cell
, vol.74
, pp. 587-590
-
-
Stahl1
Yancopoulos2
-
17
-
-
0028238769
-
Functions of the neurotrophins during nervous system development: what the knockouts are teaching us
-
(1994)
Cell
, vol.77
, pp. 627-638
-
-
Snider1
-
19
-
-
0028019114
-
Neurotrophin-6 is a new member of the nerve growth factor family
-
of special interest, Describes the isolation of a novel neurotrophin, neurotrophin (NT)-6. Extensive efforts using approaches based on the polymerase chain reaction to isolate new neurotrophins, after the rapid discovery of NT-3 and NT-4, had failed, thus suggesting that there might not be additional members of the neurotrophin family. It remains to be determined, however, whether NT-6 homologues exist in mammals.
-
(1994)
Nature
, vol.372
, pp. 266-269
-
-
Gotz1
Koster2
Winkler3
Raulf4
Lottspeich5
Schartl6
Thoenen7
-
22
-
-
0027315407
-
An extended surface of binding to Trk tyrosine kinase receptors in NGF and BDNF allows the engineering of a multifunctional panneurotrophin
-
(1993)
EMBO J
, vol.12
, pp. 2281-2293
-
-
Ibanez1
Ilag2
Murray-Rust3
Persson4
-
23
-
-
0027050178
-
Nerve growth factor mediates signal transduction through trk homodimer receptors
-
(1992)
Neuron
, vol.9
, pp. 1067-1079
-
-
Jing1
Tapley2
Barbacid3
-
24
-
-
0026578026
-
Growth factor signaling: where is the specificity?
-
(1992)
Cell
, vol.68
, pp. 995-997
-
-
Chao1
-
28
-
-
0027270865
-
trkC encodes multiple neurotrophin-3 receptors with distinct biological properties and substrate specificities
-
(1993)
EMBO J
, vol.12
, pp. 3083-3094
-
-
Lamballe1
Tapley2
Barbacid3
-
31
-
-
0025281397
-
The trkB tyrosine protein kinase gene codes for a second neurogenic receptor that lacks the catalytic kinase domain
-
(1990)
Cell
, vol.61
, pp. 647-656
-
-
Klein1
Conway2
Parada3
Barbacid4
-
37
-
-
0028293929
-
Neuronal differentiation signals are controlled by nerve growth factor receptor/Trk binding sites for SHC and PLC-γ
-
of special interest, In this paper and [36], site-directed mutagenesis was used to define the role of individual tyrosine residues in the cytoplasmic domain of the TrkA receptor. These tyrosine residues serve as specific anchors for various TrkA substrates. Therefore, the biological activity of these mutant receptors provides useful information regarding the relative contributions of these substrates (and their respective signaling pathways) to signalling by nerve growth factor.
-
(1994)
EMBO J
, vol.13
, pp. 1585-1590
-
-
Obermeier1
Bradshaw2
Seedorf3
Choidas4
Schlessinger5
Ullrich6
-
39
-
-
0027395119
-
SNT, a differentiation-specific target of neurotrophic factor-induced tyrosine kinase activity in neurons and PC12 cells
-
(1993)
Mol Cell Biol
, vol.13
, pp. 2203-2213
-
-
Rabin1
Cleghon2
Kaplan3
-
40
-
-
0028297308
-
Mice lacking nerve growth factor display perinatal loss of sensory and sympathetic neurons yet develop basal forebrain cholinergic neurons
-
of outstanding interest, Disruption of the nerve growth factor (NGF) gene by homologous recombination in embryonic stem cells results in the generation of mice that do not respond to noxious mechanical stimuli. These mice display severe loss of sensory and sympathetic neurons, confirming the critical dependence of these neurons for NGF previously shown in in vitro studies.
-
(1994)
Cell
, vol.76
, pp. 1001-1011
-
-
Crowley1
Spencer2
Nishimura3
Chen4
Pitts-Meek5
Armanini6
Ling7
McMahon8
Shelton9
Levinson10
Phillips11
-
41
-
-
0028351190
-
Targeted disruption of the BDNF gene perturbs brain and sensory neuron development but not motor neuron development
-
of outstanding interest, See [42] annotation.
-
(1994)
Cell
, vol.76
, pp. 989-999
-
-
Jones1
Farinas2
Backus3
Reichardt4
-
42
-
-
0028274040
-
Mice lacking brain-derived neurotrophic factor develop with sensory deficits
-
of outstanding interest, This study and [41] independently report the generation of mice lacking a functional brain-derived neurotrophic factor gene. Most of these mice die after birth, although some survive for 2–4 weeks, These mice display severe deficiencies in coordination and balance, a phenotype that may result from their significantly reduced levels of vestibular sensory neurons. These mice also display neuronal deficiencies in other cranial and spinal sensory ganglia, but not in motor neurons.
-
(1994)
Nature
, vol.368
, pp. 147-150
-
-
Ernfors1
Lee2
Jaenisch3
-
44
-
-
0028291238
-
Lack of neurotrophin-3 leads to deficiencies in the peripheral nervous system and loss of limb proprioceptive afferents
-
of outstanding interest, Mice lacking neurotrophin-3 die within a few weeks of birth and display abnormal limb movements. This defect is likely to be due to the lack of spinal proprioceptive afferents and muscle spindles. These mice display additional defects in other sensory (trigeminal and cochlear) and sympathetic ganglia, but not in enteric or motor neurons. In addition, the central nervous system of these mice appears to be normal, at least anatomically.
-
(1994)
Cell
, vol.77
, pp. 503-512
-
-
Ernfors1
Lee2
Kucera3
Jaenisch4
-
45
-
-
0027491104
-
Targeted disruption of the trkB neurotrophin receptor gene results in nervous system lesions and neonatal death
-
of outstanding interest, Partial disruption of the trkB gene led to the generation of mice lacking TrkB tyrosine kinase receptors but not their non-catalytic isoform gp95trkB. Most of these mice die during the first postnatal week due to lack of feeding activity. They display neuronal defects in the peripheral (trigeminal and dorsal root ganglia) and central (facial motor nucleus and spinal cord) nervous system. However, most structures of the central nervous system known to express high levels of trkB transcripts (cortex, hippocampus, etc.) appear to be normal, at least anatomically.
-
(1993)
Cell
, vol.75
, pp. 113-122
-
-
Klein1
Smeyne2
Wurst3
Long4
Auerbach5
Joyner6
Barbacid7
-
46
-
-
0028331599
-
Severe sensory and sympathetic neuropathies in mice carrying a disrupted Trk/NGF receptor gene
-
of outstanding interest, Mice lacking TrkA receptors display the same sensory and sympathetic defects as those carrying a disrupted nerve growth factor (NGF) gene, thus demonstrating that TrkA mediates NGF activity in vivo. TrkA-defective mice also display deficiencies in the cholinergic projections that connect basal forebrain neurons (known to be NGF-dependent) with the hippocampus and cortex.
-
(1994)
Nature
, vol.368
, pp. 246-249
-
-
Smeyne1
Klein2
Schnapp3
Long4
Bryant5
Lewin6
Lira7
Barbacid8
-
47
-
-
0028329355
-
Disruption of the neurotrophin-3 receptor gene trkC eliminates la muscle afferents and results in abnormal movements
-
of outstanding interest, Specific disruption of those sequences encoding the catalytic domain of the TrkC tyrosine kinase receptor results in mice with severe proprioceptive sensory defects, most likely caused by the total absence of la muscle afferent projections to spinal motor neurons. These mice also have fewer large myelinated axons in the dorsal root and posterior columns of the spinal cord. Unlike mice lacking neurotrophin-3, some of the TrkC-defective mice survive for long periods of time (〉 6 months).
-
(1994)
Nature
, vol.368
, pp. 249-251
-
-
Klein1
Silos-Santiago2
Smeyne3
Lira4
Brambilla5
Bryant6
Zhang7
Snider8
Barbacid9
-
48
-
-
0027165364
-
Nerve growth factor: a tale of two receptors
-
(1993)
Oncogene
, vol.8
, pp. 2033-2042
-
-
Barbacid1
-
54
-
-
0028270620
-
The p75 nerve growth factor receptor mediates survival or death depending on the stage of sensory neuron development
-
(1994)
Proc Natl Acad Sci USA
, vol.91
, pp. 6501-6505
-
-
Barrett1
Bartlett2
-
56
-
-
0027966170
-
Disruption of NGF binding to the low affinity neurotrophin receptor p75LNTR reduces NGF binding to TrkA on PC12 cells
-
(1994)
Neuron
, vol.13
, pp. 203-215
-
-
Barker1
Shooter2
-
57
-
-
0026747063
-
Targeted mutation of the gene encoding the low affinity NGF receptor p75 leads to deficits in the peripheral sensory nervous system
-
(1992)
Cell
, vol.69
, pp. 737-749
-
-
Lee1
Li2
Huber3
Landis4
Sharpe5
Chao6
Jaenisch7
-
58
-
-
0028294595
-
Dependence on p75 for innervation of some sympathetic targets
-
of special interest, See [59] annotation.
-
(1994)
Science
, vol.263
, pp. 1447-1449
-
-
Lee1
Bachman2
Landis3
Jaenisch4
-
59
-
-
0027330994
-
p75-deficient trigeminal sensory neurons have an altered response to NGF but not to other neurotrophins
-
of special interest, This study and [58] extend the initial characterization of the p75-null mice [57] and provide support for the concept that p75 receptors might only be indispensible for those neurons (and innervations) that have access to limiting amounts of nerve growth factor.
-
(1993)
Neuron
, vol.11
, pp. 565-574
-
-
Davies1
Lee2
Jaenisch3
-
60
-
-
0028196552
-
p75-deficient embryonic dorsal root sensory and neonatal sympathetic neurons display a decreased sensitivity to NGF
-
(1994)
Development
, vol.120
, pp. 1027-1033
-
-
Lee1
Davies2
Jaenisch3
|