research use only
Cat.No.: F6873
| Dilution |
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|
| Application |
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| WB, IP, ChIP |
| Reactivity |
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| Human, Mouse, Rat, Monkey |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 65 kDa |
| Positive Control | MCF7 cells; NIH/3T3 cells; KNRK cells; COS-7 cells |
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| Negative Control |
| Specificity |
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| COBRA1 (D6K9A) Rabbit mAb detects endogenous levels of total COBRA1 protein. |
| Clone |
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| K14G15 |
| Synonym(s) |
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| Negative elongation factor B; NELF-B; Cofactor of BRCA1; NELFB; COBRA1; KIAA1182 |
| Background |
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| COBRA1 (NELF-B), a core subunit of the Negative Elongation Factor (NELF) complex alongside WHSC2 (NELF-A), TH1L (NELF-C/D), and NELF-E, is a critical regulator of RNA polymerase II (RNAPII) transcription elongation, promoting promoter-proximal pausing in concert with DSIF and awaiting P-TEFb-mediated release through phosphorylation of both NELF and the RNAPII CTD for productive elongation. COBRA1 is predicted to adopt a HEAT repeat fold, mediating essential intersubunit interactions that anchor NELF-A and RNA-binding NELF-E, thereby stabilizing the NELF complex and facilitating its association with paused RNAPII approximately 20–60 bp downstream of promoters. COBRA1’s principal functions include maintaining RNAPII pausing to allow rapid, signal-dependent gene induction, particularly at developmental and stress-responsive genes, modulating nuclear receptor activity (estrogen, androgen, glucocorticoid receptors) to control target gene expression and alternative splicing, and negatively regulating AP-1 at promoters such as TFF1; notably, it was initially identified through its BRCT-domain interaction with the BRCA1 tumor suppressor. COBRA1 fine-tunes transcriptional output for energy metabolism genes in cardiomyocytes, governs stem cell differentiation, and modulates hormone-driven proliferation. Clinically, reduced COBRA1 expression correlates with poor prognosis in metastatic or recurrent breast cancer, whereas its overexpression promotes androgen receptor signaling and tumor growth/migration in prostate and hepatocellular cancers. |
| References |
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