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Alternative name
Deubiquitinating enzyme 28, KIAA1515, Ubiquitin thiolesterase 28, USP28 antibody
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Catalog
A009322
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Size100μg
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Formliquid
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Purity≥95% as determined by SDS-PAGE
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StoragePBS with 0.02% sodium azide and 50% glycerol pH 7.3 , -20℃ for 24 months (Avoid repeated freeze / thaw cycles.)
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ClonalityPolyclonal Antibody
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Host Rabbit
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Species ReactivityHuman,Mouse ,Rat
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Applications Tested/SuitableELISA,WB,IHC,IP
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PurificationImmunogen affinity purified
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Immunogenubiquitin specific peptidase 28
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IHCImmunohistochemistry of paraffin-embedded human breast cancer using A009322(USP28 antibody) at dilution of 1:50
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Western BlotHeLa cells were subjected to SDS PAGE followed by western blot with A009322(USP28 antibody) at dilution of 1:1000
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Recommended dilutionWB : 1:500-1:5000;IP:1：200-1：2000;IHC:1：20-1：200
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Product Description specificalDeubiquitinase involved in DNA damage response checkpoint and MYC proto-oncogene stability. Involved in DNA damage induced apoptosis by specifically deubiquitinating proteins of the DNA damage pathway such as CLSPN. Also involved in G2 DNA damage checkpoint, by deubiquitinating CLSPN, and preventing its degradation by the anaphase promoting complex/cyclosome (APC/C). In contrast, it does not deubiquitinate PLK1. Specifically deubiquitinates MYC in the nucleoplasm, leading to prevent MYC degradation by the proteasome: acts by specifically interacting with isoform 1 of FBXW7 (FBW7alpha) in the nucleoplasm and counteracting ubiquitination of MYC by the SCF(FBW7) complex. In contrast, it does not interact with isoform 4 of FBXW7 (FBW7gamma) in the nucleolus, allowing MYC degradation and explaining the selective MYC degradation in the nucleolus. Deubiquitinates ZNF304, hence preventing ZNF304 degradation by the proteasome and leading to the activated KRAS-mediated promoter hypermethylation and transcriptional silencing of tumor suppressor genes (TSGs) in a subset of colorectal cancers (CRC) cells (PubMed:24623306).
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Gene nameUSP28
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locationNucleus
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Uniprot IDQ96RU2
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Calculated M.W.130kDa
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Observed M.W.135 kDa
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