research use only
Cat.No.: F5322
| Dilution |
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|
| Application |
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| WB, IP |
| 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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| 33 kDa, 40 kDa |
| Positive Control | PC-3 cells; TK-10 cells; U031 cells; ACHN cells; HCT-15 cells; COS-7 cells; Neuro-2a cells; C6 cells; 293T cells |
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| Negative Control |
| Specificity |
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| BRCC36 Antibody [M5D3] detects endogenous levels of total BRCC36 protein. |
| Clone |
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| M5D3 |
| Synonym(s) |
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| Lys-63-specific deubiquitinase BRCC36; BRCA1/BRCA2-containing complex subunit 36; BRISC complex subunit BRCC36; BRCC3; BRCC36; C6.1A; CXorf53 |
| Background |
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| BRCC36, also known as BRCA1/BRCA2-containing complex subunit 36 or BRCC3, is a deubiquitinating enzyme from the JAMM/MPN plus metalloprotease family that specifically hydrolyzes K63-linked polyubiquitin chains to regulate ubiquitin signaling in both DNA damage repair and innate immunity. This protein is about 384 amino acids in length and contains an MPN domain with a catalytic glutamate at position 33 and an activation loop whose conformation is controlled by scaffold partners such as ABRAXAS in the BRCA1-A complex or ABRO1 in the BRISC complex. BRCC36 assembles into heteropentameric, arc-shaped complexes where it forms non-covalent dimers, and BRE provides UEV or RWD domains to bridge MERIT40 and RAP80 for full complex integration. In the BRCA1-A complex, BRCC36 is recruited to DNA double-strand break foci through RAP80’s recognition of ubiquitin, where it removes K63-linked ubiquitin chains to limit DNA end resection, suppress excessive homologous recombination, sequester BRCA1 away from breaks, and promote non-homologous end joining, thus ensuring DNA repair fidelity. In the cytoplasm, BRISC-BRCC36 deubiquitinates the type I interferon receptor IFNAR1, stabilizing it to enhance antiviral signaling and inflammatory responses, while binding to SHMT2 inhibits BRCC36 activity, linking metabolism and immunity in hypoxic tumors. Overexpression of BRCC36 contributes to breast cancer radioresistance by reducing apoptosis after DNA double-strand breaks, and its modular scaffolding allows for context-specific targeting. |
| References |
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