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A conserved rod domain phosphotyrosine that is targeted by the phosphatase PTP1B promotes keratin 8 protein insolubility and filament organization.

Snider NT, Park H, Omary MB.

J Biol Chem. 2013 Oct 25;288(43):31329-37. doi: 10.1074/jbc.M113.502724. Epub 2013 Sep 3.


Glucose and SIRT2 reciprocally mediate the regulation of keratin 8 by lysine acetylation.

Snider NT, Leonard JM, Kwan R, Griggs NW, Rui L, Omary MB.

J Cell Biol. 2013 Feb 4;200(3):241-7. doi: 10.1083/jcb.201209028. Epub 2013 Jan 28.


Protein tyrosine phosphatase 1B regulates pyruvate kinase M2 tyrosine phosphorylation.

Bettaieb A, Bakke J, Nagata N, Matsuo K, Xi Y, Liu S, AbouBechara D, Melhem R, Stanhope K, Cummings B, Graham J, Bremer A, Zhang S, Lyssiotis CA, Zhang ZY, Cantley LC, Havel PJ, Haj FG.

J Biol Chem. 2013 Jun 14;288(24):17360-71. doi: 10.1074/jbc.M112.441469. Epub 2013 May 2.


Alexander disease causing mutations in the C-terminal domain of GFAP are deleterious both to assembly and network formation with the potential to both activate caspase 3 and decrease cell viability.

Chen YS, Lim SC, Chen MH, Quinlan RA, Perng MD.

Exp Cell Res. 2011 Oct 1;317(16):2252-66. doi: 10.1016/j.yexcr.2011.06.017. Epub 2011 Jul 2.


Keratin modifications and solubility properties in epithelial cells and in vitro.

Omary MB, Ku NO, Liao J, Price D.

Subcell Biochem. 1998;31:105-40. Review.


The endless story of the glial fibrillary acidic protein.

Chen WJ, Liem RK.

J Cell Sci. 1994 Aug;107 ( Pt 8):2299-311.


Novel mutations in exon 6 of the GFAP gene affect a highly conserved if motif in the rod domain 2B and are associated with early onset infantile Alexander disease.

Hartmann H, Herchenbach J, Stephani U, Ledaal P, Donnerstag F, L├╝cke T, Das AM, Christen HJ, Hagedorn M, Meins M.

Neuropediatrics. 2007 Jun;38(3):143-7.


Keratin 18 overexpression but not phosphorylation or filament organization blocks mouse Mallory body formation.

Harada M, Strnad P, Resurreccion EZ, Ku NO, Omary MB.

Hepatology. 2007 Jan;45(1):88-96.


A new highly efficient substrate-trapping mutant of protein tyrosine phosphatase 1B (PTP1B) reveals full autoactivation of the insulin receptor precursor.

Boubekeur S, Boute N, Pagesy P, Zilberfarb V, Christeff N, Issad T.

J Biol Chem. 2011 Jun 3;286(22):19373-80. doi: 10.1074/jbc.M111.222984. Epub 2011 Apr 12.


GFAP mutations in Alexander disease.

Li R, Messing A, Goldman JE, Brenner M.

Int J Dev Neurosci. 2002 Jun-Aug;20(3-5):259-68. Review.


Investigation of protein-tyrosine phosphatase 1B function by quantitative proteomics.

Mertins P, Eberl HC, Renkawitz J, Olsen JV, Tremblay ML, Mann M, Ullrich A, Daub H.

Mol Cell Proteomics. 2008 Sep;7(9):1763-77. doi: 10.1074/mcp.M800196-MCP200. Epub 2008 May 31.


Alexander-disease mutation of GFAP causes filament disorganization and decreased solubility of GFAP.

Hsiao VC, Tian R, Long H, Der Perng M, Brenner M, Quinlan RA, Goldman JE.

J Cell Sci. 2005 May 1;118(Pt 9):2057-65. Epub 2005 Apr 19.


O-GlcNAcylation determines the solubility, filament organization, and stability of keratins 8 and 18.

Srikanth B, Vaidya MM, Kalraiya RD.

J Biol Chem. 2010 Oct 29;285(44):34062-71. doi: 10.1074/jbc.M109.098996. Epub 2010 Aug 21.


Loss of keratin 8 phosphorylation leads to increased tumor progression and correlates with clinico-pathological parameters of OSCC patients.

Alam H, Gangadaran P, Bhate AV, Chaukar DA, Sawant SS, Tiwari R, Bobade J, Kannan S, D'cruz AK, Kane S, Vaidya MM.

PLoS One. 2011;6(11):e27767. doi: 10.1371/journal.pone.0027767. Epub 2011 Nov 17.


Glial fibrillary acidic protein filaments can tolerate the incorporation of assembly-compromised GFAP-delta, but with consequences for filament organization and alphaB-crystallin association.

Perng MD, Wen SF, Gibbon T, Middeldorp J, Sluijs J, Hol EM, Quinlan RA.

Mol Biol Cell. 2008 Oct;19(10):4521-33. doi: 10.1091/mbc.E08-03-0284. Epub 2008 Aug 6.

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