ITN1980
ITN1980
- Catalog: ITN1980
- Gene/Protein: MYOC GLC1A TIGR
- Product Description: Immunotag™ MYOC Polyclonal Antibody
385.0000
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Antibody Specification | |
Datasheet | |
Target Protein | MYOC |
Clonality | Polyclonal |
Storage/Stability | -20°C/1 year |
Application | WB,ELISA |
Recommended Dilution | WB 1:500-2000 ELISA 1:5000-20000 |
Concentration | 1 mg/ml |
Reactive Species | Human,Rat,Mouse |
Host Species | Rabbit |
Immunogen | Synthesized peptide derived from part region of human protein |
Specificity | MYOC Polyclonal Antibody detects endogenous levels of protein. |
Purification | The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen |
Form | Liquid in PBS containing 50% glycerol, and 0.02% sodium azide. |
Gene Name | MYOC GLC1A TIGR |
Accession No. | Q99972 O70624 Q9R1J4 |
Description | myocilin(MYOC) Homo sapiens 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. [provided by RefSeq, Jul 2008], |
Protein Expression | Brain,Leukocyte,Retina,Stomach, |
Subcellular Localization | proteinaceous extracellular matrix,extracellular space,mitochondrial outer membrane,mitochondrial inner membrane,mitochondrial intermembrane space,endoplasmic reticulum,rough endoplasmic reticulum,Golgi apparatus,cilium,cytoplasmic, membrane-bounded vesicle, |
Protein Function | disease:Defects in MYOC are the cause of primary open angle glaucoma type 1A (GLC1A) [MIM:137750]. Primary open angle glaucoma (POAG) is characterized by a specific pattern of optic nerve and visual field defects. The angle of the anterior chamber of the eye is open, and usually the intraocular pressure is increased. The disease is asymptomatic until the late stages, by which time significant and irreversible optic nerve damage has already taken place.,disease:Defects in MYOC may also contribute to primary congenital glaucoma type 3A (GLC3A) [MIM:231300]. Defects in MYOC may contribute to this phenotype via digenic inheritance. GLC3A is an autosomal recessive form of primary congenital glaucoma (PCG). PCG is characterized by marked increase of intraocular pressure at birth or early choldhood, large ocular globes (buphthalmos) and corneal edema. It results from developmental defects of the trabecular meshwork and anterior chamber angle of the eye that prevent adequate drainage of aqueous humor.,function:May participate in the obstruction of fluid outflow in the trabecular meshwork.,PTM:Different isoforms may arise by post-translational modifications.,PTM:Glycosylated.,PTM:Palmitoylated.,similarity:Contains 1 olfactomedin-like domain.,subcellular location:Located preferentially in the ciliary rootlet and basal body of the connecting cilium of photoreceptor cells, and in the rough endoplasmic reticulum. Also secreted.,subunit:Homodimer. Interacts with OLFM3.,tissue specificity:Expressed in large amounts in various types of muscle, ciliary body, papillary sphincter, skeletal muscle, heart and other tissues. Expressed predominantly in the retina. In normal eyes, found in the inner uveal meshwork region and the anterior portion of the meshwork. In contrast, in many glaucomatous eyes, it is found in more regions of the meshwork and appeared more intensively than in normal eyes, regardless of the type or clinical severity of glaucoma., |
Usage | For Research Use Only! Not for diagnostic or therapeutic procedures. |