|Other Names||26S proteasome complex subunit DSS1, Deleted in split hand/split foot protein 1, Split hand/foot deleted protein 1, Split hand/foot malformation type 1 protein, SHFM1, DSS1, SHFDG1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP6264a was selected from the N-term region of human DSS1 . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Subunit of the 26S proteasome which plays a role in ubiquitin-dependent proteolysis (PubMed:15117943). Component of the TREX-2 complex (transcription and export complex 2), composed of at least ENY2, GANP, PCID2, DSS1, and either centrin CETN2 or CETN3 (PubMed:22307388). The TREX-2 complex functions in docking export-competent ribonucleoprotein particles (mRNPs) to the nuclear entrance of the nuclear pore complex (nuclear basket). TREX-2 participates in mRNA export and accurate chromatin positioning in the nucleus by tethering genes to the nuclear periphery. Binds and stabilizes BRCA2 and is thus involved in the control of R-loop-associated DNA damage and thus transcription- associated genomic instability. R-loop accumulation increases in DSS1-depleted cells.|
|Tissue Location||Expressed in limb bud, craniofacial primordia and skin|
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The gene for DSS1 has been localized within the split hand/split foot malformation locus SHFM1 at chromosome 7. DSS1 has been proposed to be a candidate for the autosomal dominant form of the heterogeneous limb developmental disorder split hand/split foot malformation type 1. In addition, it has been shown to directly interact with BRCA2. It also may play a role in the completion of the cell cycle.
Yang, H., et al., Science 297(5588):1837-1848 (2002).Marston, N.J., et al., Mol. Cell. Biol. 19(7):4633-4642 (1999).Jantti, J., et al., Proc. Natl. Acad. Sci. U.S.A. 96(3):909-914 (1999).Crackower, M.A., et al., Hum. Mol. Genet. 5(5):571-579 (1996).Roberts, S.H., et al., J. Med. Genet. 28(7):479-481 (1991).
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