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重組人血小板生成素受體蛋白

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產(chǎn)品編號bs-42088P
英文名稱Recombinant human TPOR protein, N-His
中文名稱重組人血小板生成素受體蛋白
別    名C MPL; C-MPL; CMPL; CD110; CD 110; MPL; MPLV; Myeloproliferative leukemia protein; Myeloproliferative leukemia virus oncogene; Proto-oncogene c-Mpl; THCYT2; Thrombopoietin receptor; TPO R; TPO-R; TPOR_HUMAN.  
理論分子量27.4kDa
性    狀Lyophilized or Liquid
濃    度>1mg/ml
物    種Human
序    列297-482/635
純    度>90% as determined by SDS-PAGE
純化方法AC
內(nèi)毒素Not analyzed
表達(dá)系統(tǒng)E.coli
活性Not tested
標(biāo)簽N-His
緩 沖 液4M Urea
保存條件Stored at -70℃ or -20℃. Avoid repeated freeze/thaw cycles.
注意事項This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
產(chǎn)品介紹In 1990 an oncogene, v-mpl, was identified from the murine myeloproliferative leukemia virus that was capable of immortalizing bone marrow hematopoietic cells from different lineages. In 1992 the human homologue, named, c-mpl, was cloned. Sequence data revealed that c-mpl encoded a protein that was homologous with members of the hematopoietic receptor superfamily. Presence of anti-sense oligodeoxynucleotides of c-mpl inhibited megakaryocyte colony formation. The ligand for c-mpl, thrombopoietin, was cloned in 1994. Thrombopoietin was shown to be the major regulator of megakaryocytopoiesis and platelet formation. The protein encoded by the c-mpl gene, CD110, is a 635 amino acid transmembrane domain, with two extracellular cytokine receptor domains and two intracellular cytokine receptor box motifs . TPO-R deficient mice were severely thrombocytopenic, emphasizing the important role of CD110 and thrombopoietin in megakaryocyte and platelet formation. Upon binding of thrombopoietin CD110 is dimerized and the JAK family of non-receptor tyrosine kinases, as well as the STAT family, the MAPK family, the adaptor protein Shc and the receptors themselves become tyrosine phosphorylated. [provided by RefSeq, Jul 2008]

SWISS:
P40238

Gene ID:
4352

產(chǎn)品圖片
The purity of the protein is greater than 90% as determined by reducing SDS-PAGE.
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