research use only
Cat.No.: F5114
| Dilution |
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|
| Application |
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| WB, IHC, IF, FCM, ELISA |
| Reactivity |
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| Human, Mouse, Rat |
| Source |
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| Mouse 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 Observed MW |
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| 75 kDa 75 kDa |
| *Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization. |
| Specificity |
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| MTA2 Antibody [P2H17] detects endogenous levels of total MTA2 protein. |
| Clone |
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| P2H17 |
| Synonym(s) |
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| Metastasis-associated protein MTA2; Metastasis-associated 1-like 1 (MTA1-L1 protein); p53 target protein in deacetylase complex; MTA2; MTA1L1; PID |
| Background |
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| MTA2 forms part of the MTA family within the NuRD chromatin remodeling and histone deacetylase complex, where it scaffolds interactions essential for transcriptional repression across diverse cellular programs. MTA2 features a zinc finger domain alongside BAH and SANT motifs that facilitate DNA and protein binding, enabling its integration into distinct NuRD variants containing MBD3, Sin3a, and CHD4 for targeted chromatin modification. Through these associations, MTA2 recruits HDAC enzymatic cores to deacetylate histones at promoter regions, compacting chromatin and silencing genes involved in differentiation and hormone response pathways. MTA2 directly engages ERα to suppress estrogen-responsive transcription, altering receptor conformation and cofactor recruitment to shift cells toward resistant phenotypes in hormone-dependent contexts. MTA2 collaborates with transcription factors like Aiolos and Ikaros in B cell progenitors, modulating lineage-specific gene networks by enforcing repressive epigenetic marks on developmental loci. This activity extends to broader lineage commitment, where MTA2-containing NuRD complexes balance progenitor proliferation against maturation cues through cyclic modulation of acetyl marks on key regulatory elements. |
| References |
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