anti-Myocilin (MYOC) Anticorps

Mouse (Murine) Myocilin (MYOC) interaction partners

1. mutant myocilin induces abnormal ECM (Montrer MMRN1 Anticorps) accumulation in the ER of TM cells, which may be responsible for reduced outflow facility and IOP elevation in myocilin-associated glaucoma.

2. Mutated myocilin and heterozygous Sod2 (Montrer SOD2 Anticorps) deficiency act synergistically in a mouse model of open-angle glaucoma

3. myocilin promotes cell proliferation and resistance to apoptosis via the ERK1/2 MAPK (Montrer MAPK1 Anticorps) signaling pathway.

4. Myocilin binds to ErbB2 (Montrer ERBB2 Anticorps)/ErbB3 (Montrer ERBB3 Anticorps), activates these receptors, and affects the downstream PI3K-AKT (Montrer AKT1 Anticorps) signaling pathway

5. Myocilin also stimulated osteogenic differentiation of wild-type MSCs, which was associated with activation of the p38 (Montrer CRK Anticorps), Erk1/2, and JNK (Montrer MAPK8 Anticorps) MAP kinase (Montrer MAPK1 Anticorps) signaling pathways

6. We suggest that intracellular myocilin plays a role as a regulator of muscle hypertrophy pathways, acting through the components of dystrophin (Montrer DMD Anticorps) associated protein complex.

7. 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.

8. 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.

9. Results do not support a causative role for increased MYOC levels or the MYOC gene in steroid-induced glaucoma.

10. Results show that myocilin and gamma-synuclein interact and as a result, myocilin's properties are changed.

Human Myocilin (MYOC) interaction partners

1. Structure and misfolding of the flexible tripartite coiled-coil domain of glaucoma-associated myocilin has been reported.

2. single nucleotide polymorphism in exon 3 of MYOC is associated with glaucoma.

3. Juvenile onset open angle glaucoma and adult onset POAG form a spectrum of phenotypes. we analyzed the common variants in MYOC and CYP1B1 (Montrer CYP1B1 Anticorps) that were shared among all the three phenotypes .An interesting finding was that, while, many CYP1B1 (Montrer CYP1B1 Anticorps) variants were found in all three types of glaucoma, there was no reported MYOC variant, that was common to all the three primary glaucomas.

4. present work reveals that FOXC1 (Montrer FOXC1 Anticorps) is an important regulator of exocytosis and establishes a new link between FOXC1 (Montrer FOXC1 Anticorps) and MYOC-associated glaucoma

5. 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.

6. The mutations c.1456C < T (p.L486F) in MYOC and c.322G < A (p.V108I) in B4GALT3 (Montrer B4GALT3 Anticorps) are likely responsible for the pathogenesis of Primary Open-angle Glaucoma in this family.

7. 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.

8. regulation by retinoic acid acts through the MYOC promoter which contains a critical cluster of four retinoic acid responsive (Montrer GPRC5A Anticorps) elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha (Montrer RARA Anticorps)/RXRalpha (Montrer RXRA Anticorps) heterodimer.

9. Five out of 30 families with PCG (16.7%) had disease attributable to CYP1B1 (Montrer CYP1B1 Anticorps) alterations suggesting that CYP1B1 (Montrer CYP1B1 Anticorps) is not the major gene causing PCG in Vietnamese unlike in the case of Arab or Romany patients.

10. The present study provides insight into the genetic or haplotype variants of MYOC and OPTN (Montrer OPTN Anticorps) genes contributing to primary glaucoma. Haplotype variants identified in the present study may be regarded as potential contributing factors of primary glaucoma in Korea.

Cow (Bovine) Myocilin (MYOC) interaction partners

1. endoproteolytic processing might regulate the activity of myocilin; the inhibition of the processing by pathogenic mutations impairs the normal role of myocilin