Genetic disorders of adipose tissue development, differentiation, and death

Annual Review of Genomics and Human Genetics

Volumn 7, Issue , 2006, Pages 175-199

  Agarwal, Anil K ^a   Garg, Abhimanyu ^a  

^a UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

Author keywords

Acyltransferases; AKT2; Lamins; Mandibuloacral dysplasia; PPAR gamma; Zinc metalloproteinase

Indexed keywords

LAMIN A; LAMIN C; NUCLEAR PROTEIN; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA; PHOSPHOLIPID; PROTEIN SERINE KINASE; TRIACYLGLYCEROL;

ADIPOCYTE; ADIPOSE TISSUE; AGPAT2 GENE; AKT2 GENE; AUTOSOMAL DOMINANT DISORDER; AUTOSOMAL RECESSIVE DISORDER; BSCL2 GENE; CELL DEATH; CELL MATURATION; CLINICAL FEATURE; DISEASE ASSOCIATION; DYSPLASIA; GENE; GENE MUTATION; GENETIC DISORDER; GENETIC HETEROGENEITY; GENETIC VARIABILITY; LIPODYSTROPHY; PHENOTYPE; PPARG GENE; REVIEW; TISSUE DIFFERENTIATION;

ADIPOSE TISSUE; CELL DEATH; CELL DIFFERENTIATION; GENETIC DISEASES, INBORN; HUMANS; LIPID METABOLISM DISORDERS; LIPODYSTROPHY;

EID: 33750310241     PISSN: 15278204     EISSN: None     Source Type: Book Series    
DOI: 10.1146/annurev.genom.7.080505.115715     Document Type: Review

References (105)

1. Aarskog D, Ose L, Pande H, Eide N. 1983. Autosomal dominant partial lipodystrophy associated with Rieger anomaly, short stature, and insulinopenic diabetes. Am. J. Med. Genet. 15:29-38
2. Agarwal AK, Arioglu E, de Almeida S, Akkoc N, Taylor SI, et al. 2002. AGPAT2 is mutated in congenital generalized lipodystrophy linked to chromosome 9q34. Nat. Genet. 31:21-23
3. Agarwal AK, Barnes RI, Garg A. 2004. Genetic basis of congenital generalized lipodystrophy. Int. J. Obes. Relat. Metab. Disord. 28:336-39
4. Agarwal AK, Barnes RI, Garg A. 2006. Functional characterization of human 1-acylglycerol-3-phosphate acyltransferase isoform 8: cloning, tissue distribution, gene structure and enzymatic activity. Arch. Biochem. Biophys. 449:64-76
5. Agarwal AK, Fryns JP, Auchus RJ, Garg A. 2003. Zinc metalloproteinase, ZMP-STE24, is mutated in mandibuloacral dysplasia. Hum. Mol. Genet. 12:1995-2001
6. Agarwal AK, Garg A. 2002. A novel heterozygous mutation in peroxisome proliferator-activated receptor-γ gene in a patient with familial partial lipodystrophy. J. Clin. Endocrinol. Metab. 87:408-11
7. Agarwal AK, Garg A. 2003. Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathways. Trends Endocrinol. Metab. 14:214-21
8. Agarwal AK, Garg A. 2004. Seipin: a mysterious protein. Trends Mol. Med. 10:440-44
9. Agarwal AK, Garg A. 2006. Genetic basis of lipodystrophies and management of metabolic complications. Annu. Rev. Med. 5:297-311
10. Agarwal AK, Simha V, Oral EA, Moran SA, Gorden P, et al. 2003. Phenotypic and genetic heterogeneity in congenital generalized lipodystrophy. J. Clin. Endocrinol. Metab. 88:4840-47
11. Agarwal AK, Zhou XJ, Hall RK, Nicholls K, Bankier A, Van Esch H, Fryns JP, Garg A. 2006. Focal segmental glomerulosclerosis in patients with mandibuloacral dysplasia due to ZMPSTE24 deficiency. J. Investig. Med. In press
12. Al-Shali K, Cao H, Knoers N, Hermus AR, Tack CJ, Hegele RA. 2004. A single-base mutation in the peroxisome proliferator-activated receptor gamma4 promoter associated with altered in vitro expression and partial lipodystrophy. J. Clin. Endocrinol. Metab. 89:5655-60
13. Arimura T, Helbling-Leclerc A, Massart C, Varnous S, Niel F, et al. 2005. Mouse model carrying H222P-Lmna mutation develops muscular dystrophy and dilated cardiomyopathy similar to human striated muscle laminopathies. Hum. Mol. Genet. 14:155-69
14. Bankier A, Keith CG, Temple IK. 1995. Absent iris stroma, narrow body build and small facial bones: a new association or variant of SHORT syndrome? Clin. Dysmorphol. 4:304-12
15. Barak Y, Nelson MC, Ong ES, Jones YZ, Ruiz-Lozano P, et al. 1999. PPAR gamma is required for placental, cardiac, and adipose tissue development. Mol. Cell 4:585-95
16. Berardinelli W. 1954. An undiagnosed endocrinometabolic syndrome: report of two cases. J. Clin. Endocrinol. Metab. 14:193-204
17. Bergo MO, Gavino B, Ross J, Schmidt WK, Hong C, et al. 2002. Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. Proc. Natl. Acad. Sci. USA 99:13049-54
18. Bonne G, Di Barletta MR, Varnous S, Becane HM, Hammouda EH, et al. 1999. Mutations in the gene encoding lamin A/C cause autosomal dominant Emery-Dreifuss muscular dystrophy. Nat. Genet. 21:285-88
19. Brunner HG, van Driel MA. 2004. From syndrome families to functional genomics. Nat. Rev. Genet. 5:545-51
20. Burke B, Stewart CL. 2002. Life at the edge: the nuclear envelope and human disease. Nat. Rev. Mol. Cell Biol. 3:575-85
21. Cao H, Hegele RA. 2000. Nuclear lamin A/C R482Q mutation in Canadian kindreds with Dunnigan-type familial partial lipodystrophy. Hum. Mol. Genet. 9:109-12
22. Cao H, Hegele RA 2003. LMNA is mutated in Hutchinson-Gilford progeria (MIM 176670) but not in Wiedemann-Rautenstrauch progeroid syndrome (MIM 264090). J. Hum. Genet. 48:271-74
23. Caux F, Dubosclard E, Lascols O, Buendia B, Chazouilleres O, et al. 2003. A new clinical condition linked to a novel mutation in lamins A and C with generalized lipoatrophy, insulin-resistant diabetes, disseminated leukomelanodermic papules, liver steatosis, and cardiomyopathy. J. Clin. Endocrinol. Metab. 88:1006-13
24. Chandalia M, Garg A, Vuitch F, Nizzi F. 1995. Postmortem findings in congenital generalized lipodystrophy. J. Clin. Endocrinol. Metab. 80:3077-81
25. Chen L, Lee L, Kudlow BA, Dos Santos HG, Sletvold O, et al. 2003. LMNA mutations in atypical Werner's syndrome. Lancet 362:440-45
26. Cutler DA, Sullivan T, Marcus-Samuels B, Stewart CL, Reitman ML. 2002. Characterization of adiposity and metabolism in Lmna-deficient mice. Biochem. Biophys. Res. Commun. 291:522-27
27. De Sandre-Giovannoli A, Chaouch M, Kozlov S, Vallat JM, Tazir M, et al. 2002. Homozygous defects in LMNA, encoding lamin A/C nuclear-envelope proteins, cause autosomal recessive axonal neuropathy in human (Charcot-Marie-Tooth disorder type 2) and mouse. Am. J. Hum. Genet. 70:726-36
28. Denecke J, Brune T, Feldhaus T, Robenek H, Kranz C, et al. 2006. A homozygous ZMPSTE24 null mutation in combination with a heterozygous mutation in the LMNA gene causes Hutchinson-Gilford Progeria Syndrome (HGPS): Insights into the pathophysiology of HGPS. Hum. Mutat. 27:524-31
29. di Barletta M, Ricci E, Galluzzi G, Tonali P, Mora M, et al. 2000. Différent mutations in the LMNA gene cause autosomal dominant and autosomal recessive Emery-Dreifuss muscular dystrophy. Am. J. Hum. Genet. 66:1407-12
30. Draper N, Walker EA, Bujalska IJ, Tomlinson JW, Chalder SM, et al. 2003. Mutations in the genes encoding 11β-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase deficiency. Nat. Genet. 34:434-39
31. Dunnigan MG, Cochrane MA, Kelly A, Scott JW. 1974. Familial lipoatrophic diabetes with dominant transmission. A new syndrome. Q. J. Med. 43:33-48
32. Eberhardt C, Gray PW, Tjoelker LW. 1997. Human lysophosphatidic acid acyltransferase. cDNA cloning, expression, and localization to chromosome 9q34.3. J. Biol. Chem. 272:20299-305
33. Eberhardt C, Gray PW, Tjoelker LW. 1999. cDNA cloning, expression and chromosomal localization of two human lysophosphatidic acid acyltransferases. Adv. Exp. Med. Biol. 469:351-56
34. Eriksson M, Brown WT, Gordon LB, Glynn MW, Singer J, et al. 2003. Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature 423:293-98
35. Esteller M, Almouzni G. 2005. How epigenetics integrates nuclear functions. Workshop on epigenetics and chromatin: transcriptional regulation and beyond. EMBO Rep. 6:624-28
36. Fisher DZ, Chaudhary N, Blobel G. 1986. cDNA sequencing of nuclear lamins A and C reveals primary and secondary structural homology to intermediate filament proteins. Proc. Natl. Acad. Sci. USA 83:6450-54
37. Fleckenstein JL, Garg A, Bonte FJ, Vuitch MF, Peshock RM. 1992. The skeleton in congenital, generalized lipodystrophy: evaluation using whole-body radiographic surveys, magnetic resonance imaging and technetium-99m bone scintigraphy. Skeletal Radiol. 21:381-86
38. Fong LG, Frost D, Meta M, Qiao X, Yang SH, et al. 2006. A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeria. Science 311:1621-23
39. Fraga MF, Ballestar E, Paz MF, Ropero S, Setien F, et al. 2005. Epigenetic differences arise during the lifetime of monozygotic twins. Proc. Natl. Acad. Sci. USA 102:10604-9
40. Garg A. 2000. Gender differences in the prevalence of metabolic complications in familial partial lipodystrophy (Dunnigan variety). J. Clin. Endocrinol. Metab. 85:1776-82
41. Garg A. 2004. Acquired and genetic lipodystrophies. N. Engl. J. Med. 350:1220-34
42. Garg A, Cogulu O, Ozkinay F, Onay H, Agarwal AK. 2005. A novel homozygous Ala529Val LMNA mutation in Turkish patients with mandibuloacral dysplasia. J. Clin, Endocrinol. Metab. 90:5259-64
43. Garg A, Fleckenstein JL, Peshock RM, Grundy SM. 1992. Peculiar distribution of adipose tissue in patients with congenital generalized lipodystrophy. J. Clin. Endocrinol. Metab. 75:358-61
44. Garg A, Misra A. 2004. Lipodystrophies: rare disorders causing metabolic syndrome. Endocrinol. Metab. Clin. North Am. 33:305-31
45. Garg A, Peshock RM, Fleckenstein JL. 1999. Adipose tissue distribution pattern in patients with familial partial lipodystrophy (Dunnigan variety). J. Clin. Endocrinol. Metab. 84:170-74
46. Garg A, Speckman RA, Bowcock AM. 2002. Multisystem dystrophy syndrome due to novel missense mutations in the amino terminal head and α-helical rod domain of the lamin A/C (LMNA) gene. Am. J. Med. 112:549-55
47. Garg A, Vinaitheerthan M, Weatherall P, Bowcock A. 2001. Phenotypic heterogeneity in patients with familial partial lipodystrophy (Dunnigan variety) related to the site of mis-sense mutations in Lamin A/C (LMNA) gene. J. Clin. Endocrinol. Metab. 86:59-65
48. Garg A, Wilson R, Barnes R, Arioglu E, Zaidi Z, et al. 1999. A gene for congenital generalized lipodystrophy maps to human chromosome 9q34. J. Clin. Endocrinol. Metab. 84:3390-94
49. Garofalo RS, Orena SJ, Rafidi K, Torchia AJ, Stock JL, et al. 2003. Severe diabetes, age-dependent loss of adipose tissue, and mild growth deficiency in mice lacking Akt2/PKB beta. J. Clin. Invest. 112:197-208
50. George S, Rochford JJ, Wolfrum C, Gray SL, Schinner S, et al. 2004. A family with severe insulin resistance and diabetes due to a mutation in AKT2. Science 304:1325-28
51. Giallourakis C, Henson C, Reich M, Xie X, Mootha VK. 2005. Disease gene discovery through integrative genomics. Annu. Rev. Genomics Hum. Genet. 6:381-406
52. Gorlin RJ, Cervenka J, Moller K, Horrobin M, Witkop J. 1975. Rieger anomaly and growth retardation (The S-H-O-R-T Syndrome). Birth Defects 11:46-48
53. Haque W, Garg A, Agarwal AK. 2005. Enzymatic activity of naturally occurring 1-acylglycerol-3-phosphate-O-acyltransferase 2 mutants associated with congenital generalized lipodystrophy. Biochem. Biophys. Res. Commun. 327:446-53
54. Haque WA, Oral EA, Dietz K, Bowcock AM, Agarwal AK, Garg A. 2003. Risk factors for diabetes mellitus in familial partial lipodystrophy, Dunnigan variety. Diabetes Care 26:1350-55
55. Haque WA, Shimomura I, Matsuzawa Y, Garg A. 2002. Serum adiponectin and leptin levels in patients with lipodystrophies. J. Clin. Endocrinol. Metab. 87:2395-98
56. Hegele RA. 2001. Premature atherosclerosis associated with monogenic insulin resistance. Circulation 103:2225-29
57. Hegele RA, Cao H, Frankowski C, Mathews ST, Leff T. 2002. PPARG F388L, a transactivation-deficient mutant, in familial partial lipodystrophy. Diabetes 51:3586-90
58. Herbst KL, Tannock LR, Deeb SS, Purnell JQ, Brunzell JD, Chait A. 2003. Kobberling type of familial partial lipodystrophy: an underrecognized syndrome. Diabetes Care 26:1819-24
59. Jacob KN, Baptista F, Dos Santos HG, Oshima J, Agarwal AK, Garg A. 2005. Phenotypic heterogeneity in body fat distribution in patients with atypical Werner's syndrome due to heterozygous Arg133Leu Lamin A/C mutation. J. Clin. Endocrinol. Metab. 90:6699-706.
60. Korniszewski L, Nowak R, Okninska-Hoffmann E, Skorka A, Gieruszczak-Bialek D, Sawadro-Rochowska M. 2001. Wiedemann-Rautenstrauch (neonatal progeroid) syndrome: new case with normal telomere length in skin fibroblasts. Am. J. Med. Genet. 103:144-48
61. Kubota N, Terauchi Y, Miki H, Tamemoto H, Yamauchi T, et al. 1999. PPAR gamma mediates high-fat diet-induced adipocyte hypertrophy and insulin resistance. Mol. Cell 4:597-609
62. Leung DW. 2001. The structure and functions of human lysophosphatidic acid acyltransferases. Front. Biosci. 6:d944-53
63. Li D, Yu L, Wu H, Shan Y, Guo J, et al. 2003. Cloning and identification of the human LPAAT-zeta gene, a novel member of the lysophosphatidic acid acyltransferase family. J. Hum. Genet. 48:438-42
64. Lin F, Worman HJ. 1993. Structural organization of the human gene encoding nuclear lamin A and nuclear lamin C. J. Biol. Chem. 268:16321-26
65. Mager J, Bartolomei MS. 2005. Strategies for dissecting epigenetic mechanisms in the mouse. Nat. Genet. 37:1194-200
66. Magre J, Delepine M, Khallouf E, Gedde-Dahl T Jr, Van Maldergem L, et al. 2001. Identification of the gene altered in Berardinelli-Seip congenital lipodystrophy on chromosome 11q13. Nat. Genet. 28:365-70
67. 66a. Magre J, Delepine M, Van Maldergem L, Robert JJ, Maassen JA, et al. 2003. Prevalence of mutations in AGPAT2 among human lipodystrophies. Diabetes 52:1573-638
68. Miles PD, Barak Y, He W, Evans RM, Olefsky JM. 2000. Improved insulin-sensitivity in mice heterozygous for PPAR-gamma deficiency. J. Clin. Invest. 105:287-92
69. Mounkes LC, Kozlov S, Hernandez L, Sullivan T, Stewart CL. 2003. A progeroid syndrome in mice is caused by defects in A-type lamins. Nature 423:298-301
70. Mounkes LC, Kozlov SV, Rottman JN, Stewart CL. 2005. Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice. Hum. Mol. Genet. 14:2167-80
71. Muchir A, Bonne G, van der Kooi AJ, van Meegen M, Baas F, et al. 2000. Identification of mutations in the gene encoding lamins A/C in autosomal dominant limb girdle muscular dystrophy with atrioventricular conduction disturbances (LGMD1B). Hum. Mol. Genet. 9:1453-59
72. Novelli G, Muchir A, Sangiuolo F, Helbling-Leclerc A, D'Apice MR, et al. 2002. Mandibuloacral dysplasia is caused by a mutation in LMNA-encoding lamin A/C. Am. J. Hum. Genet. 71:426-31
73. Oral EA, Simha V, Ruiz E, Andewelt A, Premkumar A, et al. 2002. Leptin-replacement therapy for lipodystrophy. N. Engl. J. Med. 346:570-578
74. Pakendorf B, Stoneking M. 2005. Mitochondrial DNA and human evolution. Annu. Rev. Genomics Hum. Genet. 6:165-83
75. Pardini VC, Victoria IM, Rocha SM, Andrade DG, Rocha AM, et al. 1998. Leptin levels, β-cell function, and insulin sensitivity in families with congenital and acquired generalized lipoatrophic diabetes. J. Clin. Endocrinol. Metab. 83:503-8
76. Pendas AM, Zhou Z, Cadinanos J, Freije JM, Wang J, et al. 2002. Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice. Nat. Genet. 31:94-99
77. Peters JM, Barnes R, Bennett L, Gitomer WM, Bowcock AM, Garg A. 1998. Localization of the gene for familial partial lipodystrophy (Dunnigan variety) to chromosome 1q21-22. Nat. Genet. 18:292-95
78. Pivnick EK, Angle B, Kaufman RA, Hall BD, Pitukcheewanont P, et al. 2000. Neonatal progeroid (Wiedemann-Rautenstrauch) syndrome: report of five new cases and review. Am. J. Med. Genet 90:131-40
79. Plasilova M, Chattopadhyay C, Pal P, Schaub NA, Buechner SA, et al. 2004. Homozygous missense mutation in the lamin A/C gene causes autosomal recessive Hutchinson-Gilford progeria syndrome. J. Med. Genet. 41:609-14
80. Rautenstrauch T, Snigula F, Krieg T, Gay S, Muller PK. 1971. Progeria: a cell culture study and clinical report of familial incidence. Eur. J. Pediatr. 124:101-11
81. Rosen ED, Sarraf P, Troy AE, Bradwin G, Moore K, et al. 1999. PPAR gamma is required for the differentiation of adipose tissue in vivo and in vitro. Mol. Cell 4:611-17
82. Savage DB, Agostini M, Barroso I, Gurnell M, Luan J, et al. 2002. Digenic inheritance of severe insulin resistance in a human pedigree. Nat. Genet. 31:379-84
83. Savage DB, Tan GD, Acerini CL, Jebb SA, Agostini M, et al. 2003. Human metabolic syndrome resulting from dominant-negative mutations in the nuclear receptor peroxisome proliferator-activated receptor-γ. Diabetes 52:910-17
84. Seip M. 1959. Lipodystrophy and gigantism with associated endocrine manifestations: a new diencephalic syndrome? Acta Paediatr. 48:555-74
85. Seip M, Trygstad O. 1996. Generalized lipodystrophy, congenital and acquired (lipoatrophy). Acta Paediatrica. Suppl. 413:2-28
86. Sensenbrenner JA, Hussels IE, Levin LS. 1975. CC: a low birthweight syndrome, Rieger syndrome. Birth Defects 11:423-26
87. Shackleton S, Lloyd DJ, Jackson SN, Evans R, Niermeijer MF, et al. 2000. LMNA, encoding lamin A/C, is mutated in partial lipodystrophy. Nat. Genet. 24:153-56
88. Shackleton S, Smallwood DT, Clayton P, Wilson LC, Agarwal AK, et al. 2005. Compound heterozygous ZMPSTE24 mutations reduce prelamin A processing and result in a severe progeroid phenotype. J. Med. Genet. 42:e36
89. Simha V, Agarwal AK, Oral EA, Fryns JP, Garg A. 2003. Genetic and phenotypic heterogeneity in patients with mandibuloacral dysplasia-associated lipodystrophy. J. Clin. Endocrinol. Metab. 88:2821-24
90. Simha V, Garg A. 2002. Body fat distribution and metabolic derangements in patients with familial partial lipodystrophy associated with mandibuloacral dysplasia. J. Clin. Endocrinol. Metab. 87:776-85
91. Simha V, Garg A. 2003. Phenotypic heterogeneity in body fat distribution in patients with congenital generalized lipodystrophy due to mutations in the AGPAT2 or Seipin genes. J. Clin. Endocrinol. Metab. 88:5433-37
92. Sinensky M, Fantle K, Trujillo M, McLain T, Kupfer A, Dalton M. 1994. The processing pathway of prelamin A. J. Cell Sci. 107(Pt. 1):61-67
93. Song G, Ouyang G, Bao S. 2005. The activation of Akt/PKB signaling pathway and cell survival. J. Cell Mol. Med. 9:59-71
94. Sorge G, Ruggieri M, Polizzi A, Scuderi A, Di Pietro M. 1996. SHORT syndrome: a new case with probable autosomal dominant inheritance. Am. J. Med. Genet 61:178-81
95. Speckman RA, Garg A, Du F, Bennett L, Veile R, et al. 2000. Mutational and haplotype analyses of families with familial partial lipodystrophy (Dunnigan variety) reveal recurrent missense mutations in the globular C-terminal domain of lamin A/C. Am. J. Hum. Genet. 66:1192-98
96. Sullivan T, Escalante-Alcalde D, Bhatt H, Anver M, Bhat N, et al. 1999. Loss of A-type lamin expression compromises nuclear envelope integrity leading to muscular dystrophy. J. Cell Biol. 147:913-20
97. Tsai YS, Kim HJ, Takahashi N, Kim HS, Hagaman JR, et al. 2004. Hypertension and abnormal fat distribution but not insulin resistance in mice with P465L PPARgamma. J. Clin. Invest. 114:240-49
98. Tsai YS, Maeda N. 2005. PPARgamma: a critical determinant of body fat distribution in humans and mice. Trends Cardiovasc. Med. 15:81-85
99. Van Maldergem L, Magre J, Khallouf TE, Gedde-Dahl T Jr, Delepine M, et al. 2002. Genotype-phenotype relationships in Berardinelli-Seip congenital lipodystrophy. J. Med. Genet. 39:722-33
100. Vigouroux C, Magre J, Vantyghem MC, Bourut C, Lascols O, et al. 2000. Lamin A/C gene: sex-determined expression of mutations in Dunnigan-type familial partial lipodystrophy and absence of coding mutations in congenital and acquired generalized lipoatrophy. Diabetes 49:1958-62
101. West J, Tompkins CK, Balantac N, Nudelman E, Meengs B, et al. 1997. Cloning and expression of two human lysophosphatidic acid acyltransferase cDNAs that enhance cytokine-induced signaling responses in cells. DNA Cell Biol. 16:691-701
102. Wiedemann HR. 1979. An unidentified neonatal progeroid syndrome: follow-up report. Eur. J. Pediatr. 130:65-70
103. Windpassinger C, Auer-Grumbach M, Irobi J, Patel H, Petek E, et al. 2004. Heterozygous missense mutations in BSCL2 are associated with distal hereditary motor neuropathy and Silver syndrome. Nat. Genet. 36:271-76
104. Ye GM, Chen C, Huang S, Han DD, Guo JH, et al. 2005. Cloning and characterization a novel human 1-acyl-sn-glycerol-3-phosphate acyltransferase gene AGPAT7. DNA Sequation 16:386-90
105. Young SG, Fong LG, and Michaelis S. 2005. Prelamin A, Zmpste24, misshapen cell nuclei, and progeria: new evidence suggesting that protein farnesylation could be important for disease pathogenesis. J. Lipid Res. 46:2531-58