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MYOC encodes the protein myocilin, which is believed to have a role in cytoskeletal function. Additionally we are shipping Myocilin Antibodies (58) and Myocilin Kits (6) and many more products for this protein.
Showing 10 out of 23 products:
Human MYOC Protein expressed in Human Cells - ABIN2005424
Kubota, Noda, Wang, Minoshima, Asakawa, Kudoh, Mashima, Oguchi, Shimizu: A novel myosin-like protein (myocilin) expressed in the connecting cilium of the photoreceptor: molecular cloning, tissue expression, and chromosomal mapping. in Genomics 1997
Show all 5 references for ABIN2005424
Human MYOC Protein expressed in HEK-293 Cells - ABIN2181527
Kwon, Fingert, Kuehn, Alward: Primary open-angle glaucoma. in The New England journal of medicine 2009
Mutated myocilin and heterozygous Sod2 (show SOD2 Proteins) deficiency act synergistically in a mouse model of open-angle glaucoma
myocilin promotes cell proliferation and resistance to apoptosis via the ERK1/2 MAPK (show MAPK1 Proteins) signaling pathway.
Myocilin binds to ErbB2 (show ERBB2 Proteins)/ErbB3 (show ERBB3 Proteins), activates these receptors, and affects the downstream PI3K-AKT (show AKT1 Proteins) signaling pathway
Myocilin also stimulated osteogenic differentiation of wild-type MSCs, which was associated with activation of the p38 (show CRK Proteins), Erk1/2, and JNK (show MAPK8 Proteins) MAP kinase (show MAPK1 Proteins) signaling pathways
We suggest that intracellular myocilin plays a role as a regulator of muscle hypertrophy pathways, acting through the components of dystrophin (show DMD Proteins) associated protein complex.
The TIGR is implicated in resistance to oxidative stress. Despite the presence of a SOD motif, which is necessary for protection in mammalian cells, the protein is not a functional SOD, but might be involved in SOD activity.
TIGR is a newly identified component of the CNS glial scar that is likely to contribute to neuronal regenerative failure characteristic of the mammalian CNS.
Results do not support a causative role for increased MYOC levels or the MYOC gene in steroid-induced glaucoma.
Results show that myocilin and gamma-synuclein (show SNCG Proteins) interact and as a result, myocilin's properties are changed.
These data suggest that production, apparent misfolding, and nonsecretion of mutant MYOC are not, by themselves, sufficient to cause glaucoma in vivo.
Familial linkage studies for primary angle-closure glaucoma have been performed and identified MYOC causative primary angle-closure glaucoma disease
The rate of CYP1B1 (show CYP1B1 Proteins) mutations in Lebanese patients with primary congenital glaucoma (PCG) is lower than that reported in other Arab and Middle Eastern populations and suggests other genes are responsible.
Data show that predictive genetic testing for early onset Myocilin glaucoma can facilitate early detection of disease or discharge from routine ophthalmic examinations.
This study does not confirm a role for genetic variants in the MYOC, NR3C1 (show NR3C1 Proteins) and FKBP5 (show FKBP5 Proteins) genes in the pathogenesis of corticosteroid-induced ocular hypertension.
Glaucomatous MYOC mutations activate the IL-1beta (show IL1B Proteins)/NF-kappaB (show NFKB1 Proteins) inflammatory stress response and the glaucoma marker SELE (show SELE Proteins) in trabecular meshwork cells.
Secondary structure prediction of the Ser341Pro MYOC gene mutation suggested that the MYOC protein was misfolded.
Mutations in myoc ofactomedin domain are causative in the autosomal dominant inherited form of the prevalent ocular disorder glaucoma.
A novel heterozygous missense mutation c.761CMYOC gene was identified as being co-segregated with the primary open-angle glaucoma phenotype in this family.
All POAG samples underwent full sequencing of the MYOC gene, and we found a sensitivity of 100%, specificity of 99.91%, positive predictive value of 95.65%, and negative predictive value of 100% between imputation and sequencing.
FAs (show FAS Proteins), expression of fibrogenic markers, and myocilin in HTM cells. These characteristics of Hic-5 (show TGFB1I1 Proteins) in TM cells indicate its importance in regulation of AH outflow through the TM in both normal and glaucomatous eyes.
endoproteolytic processing might regulate the activity of myocilin; the inhibition of the processing by pathogenic mutations impairs the normal role of myocilin
MYOC encodes the protein myocilin, which is believed to have a role in cytoskeletal function. MYOC is expressed in many occular tissues, including the trabecular meshwork, and was revealed to be the trabecular meshwork glucocorticoid-inducible response protein (TIGR). The trabecular meshwork is a specialized eye tissue essential in regulating intraocular pressure, and mutations in MYOC have been identified as the cause of hereditary juvenile-onset open-angle glaucoma.
, trabecular meshwork-induced glucocorticoid response protein
, mutated trabecular meshwork-induced glucocorticoid response protein