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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 (59) and Myocilin Kits (6) and many more products for this protein.
Showing 10 out of 23 products:
mutant myocilin induces abnormal ECM (show MMRN1 Proteins) accumulation in the ER of TM cells, which may be responsible for reduced outflow facility and IOP elevation in myocilin-associated glaucoma.
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 interact and as a result, myocilin's properties are changed.
present work reveals that FOXC1 (show FOXC1 Proteins) is an important regulator of exocytosis and establishes a new link between FOXC1 (show FOXC1 Proteins) and MYOC-associated glaucoma
The four detected MYOC mutations appeared to be associated with morphologic changes in the trabecular meshwork and the underlying pathogenesis of a subtype of familial primary open angle glaucoma.
The mutations c.1456C < T (p.L486F) in MYOC and c.322G < A (p.V108I) in B4GALT3 (show B4GALT3 Proteins) are likely responsible for the pathogenesis of Primary Open-angle Glaucoma in this family.
Our findings demonstrated that MYOC cascade genetic testing for POAG allows identification of at-risk individuals at an early stage or even before signs of glaucoma are present. To our knowledge, this is the first study to demonstrate the clinical utility of predictive genetic testing for MYOC glaucoma.
regulation by retinoic acid acts through the MYOC promoter which contains a critical cluster of four retinoic acid responsive (show GPRC5A Proteins) elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha (show RARA Proteins)/RXRalpha (show RXRA Proteins) heterodimer.
Five out of 30 families with PCG (16.7%) had disease attributable to CYP1B1 (show CYP1B1 Proteins) alterations suggesting that CYP1B1 (show CYP1B1 Proteins) is not the major gene causing PCG in Vietnamese unlike in the case of Arab or Romany patients.
The present study provides insight into the genetic or haplotype variants of MYOC and OPTN (show OPTN Proteins) genes contributing to primary glaucoma. Haplotype variants identified in the present study may be regarded as potential contributing factors of primary glaucoma in Korea.
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.
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