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MYOC encodes the protein myocilin, which is believed to have a role in cytoskeletal function. Zusätzlich bieten wir Ihnen Myocilin Antikörper (58) und Myocilin Kits (6) und viele weitere Produktgruppen zu diesem Protein an.
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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
Zeige alle 5 Referenzen für 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
mutant myocilin induces abnormal ECM (zeige MMRN1 Proteine) 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 (zeige SOD2 Proteine) deficiency act synergistically in a mouse model of open-angle glaucoma
myocilin promotes cell proliferation and resistance to apoptosis via the ERK1/2 MAPK (zeige MAPK1 Proteine) signaling pathway.
Myocilin binds to ErbB2 (zeige ERBB2 Proteine)/ErbB3 (zeige ERBB3 Proteine), activates these receptors, and affects the downstream PI3K-AKT (zeige AKT1 Proteine) signaling pathway
Myocilin also stimulated osteogenic differentiation of wild-type MSCs, which was associated with activation of the p38 (zeige CRK Proteine), Erk1/2, and JNK (zeige MAPK8 Proteine) MAP kinase (zeige MAPK1 Proteine) signaling pathways
We suggest that intracellular myocilin plays a role as a regulator of muscle hypertrophy pathways, acting through the components of dystrophin (zeige DMD Proteine) 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 (zeige SNCG Proteine) interact and as a result, myocilin's properties are changed.
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 (zeige GPRC5A Proteine) elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha (zeige RARA Proteine)/RXRalpha (zeige RXRA Proteine) heterodimer.
Five out of 30 families with PCG (16.7%) had disease attributable to CYP1B1 (zeige CYP1B1 Proteine) alterations suggesting that CYP1B1 (zeige CYP1B1 Proteine) 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 (zeige OPTN Proteine) 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 (zeige CYP1B1 Proteine) 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 (zeige NR3C1 Proteine) and FKBP5 (zeige FKBP5 Proteine) genes in the pathogenesis of corticosteroid-induced ocular hypertension.
Glaucomatous MYOC mutations activate the IL-1beta (zeige IL1B Proteine)/NF-kappaB (zeige NFKB1 Proteine) inflammatory stress response and the glaucoma marker SELE (zeige SELE Proteine) in trabecular meshwork cells.
Secondary structure prediction of the Ser341Pro MYOC gene mutation suggested that the MYOC protein was misfolded.
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