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Connexin 26 Rabbit pAb
- 产品详情
- 实验流程
Application 
| WB, IHC-P, IHC-F, IF, E |
|---|---|
| Primary Accession | P29033 |
| Other Accession | P29033 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 26215 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human Connexin-26 |
| Epitope Specificity | 81-180/226 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SIMILARITY | Belongs to the connexin family. Alpha-type (group II) subfamily. |
| Post-translational modifications | Belongs to the connexin family. Beta-type (group I) subfamily. |
| DISEASE | Defects in GJA1 are the cause of autosomal dominant oculodentodigital dysplasia (ODDD) [MIM:164200]; also known as oculodentoosseous dysplasia. ODDD is a highly penetrant syndrome presenting with craniofacial (ocular, nasal, dental) and limb dysmorphisms, spastic paraplegia, and neurodegeneration. Craniofacial anomalies tipically include a thin nose with hypoplastic alae nasi, small anteverted nares, prominent columnella, and microcephaly. Brittle nails and hair abnormalities of hypotrichosis and slow growth are present. Ocular defects include microphthalmia, microcornea, cataracts, glaucoma, and optic atrophy. Syndactyly type 3 and conductive deafness can occur in some cases. Cardiac abnormalities are observed in rare instances. Defects in GJA1 are the cause of autosomal recessive oculodentodigital dysplasia (ODDD autosomal recessive) [MIM:257850]. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | Gap junction channels consist of connexin protein subunits, which are encoded by a multigene family. GJBs (gap junction proteins or connexins) play crucial functional roles associated with these channels. Immunohistochemical staining of human cochlear cells demonstrated high levels of GJB2 expression. Mutations in GJB2 are associated with genetically derived hearing impairments, including autosomal recessive nonsyndromic deafness. |
| Gene ID | 2706 |
|---|---|
| Other Names | BAPS; CX26; DFNA3; DFNA3A; DFNB1; DFNB1A; HID; KID; NSRD1; PPK; Cnx26; Cxne; Gjb-2; CXN-26; CXB2_HUMAN; GJB2; Connexin-26 (Cx26); CXB2_MOUSE; CXB2_RAT; gap junction protein beta 2; gap junction protein, beta 2, 26kD (connexin 26); gap junction protein, beta 2, 26kDa (connexin 26); gap junction protein, beta 2, 26kDa; connexin 26 |
| Dilution | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,ELISA=1:5000-10000 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | GJB2 |
|---|---|
| Function | Structural component of gap junctions (PubMed:16849369, PubMed:17551008, PubMed:19340074, PubMed:19384972, PubMed:21094651, PubMed:26753910). Gap junctions are dodecameric channels that connect the cytoplasm of adjoining cells. They are formed by the docking of two hexameric hemichannels, one from each cell membrane (PubMed:17551008, PubMed:19340074, PubMed:21094651, PubMed:26753910). Small molecules and ions diffuse from one cell to a neighboring cell via the central pore (PubMed:16849369, PubMed:19384972, PubMed:21094651). |
| Cellular Location | Cell membrane; Multi-pass membrane protein. Cell junction, gap junction. Note=Colocalizes with GJB4 at gap junction plaques in the cochlea. {ECO:0000250|UniProtKB:Q00977} |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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¥ 1,250.00
Cat# AP97301
