CDT2 Antibody Blocking Peptide(bs-7935P)-500ug

CDT2 Antibody Blocking Peptide

(bs-7935P)-500ug
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  • ¥880
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  • bs-7935P
  • 2025年10月16日
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      500ug

    产品编号bs-7935P
    英文名称CDT2 Antibody Blocking Peptide
    中文名称维甲酸调节核基质相关蛋白封闭多肽
    英文别名Lethal(2) denticleless protein homolog; CDW1; CDW1; DCAF2; DDB1 and CUL4 associated factor 2; Ddb1- and Cul4-associated factor 2; Denticleless homolog; Denticleless homolog (Drosophila); Denticleless protein homolog; Dtl; DTL_HUMAN; L2DTL; Lethal(2) denticleless protein homolog; RA regulated nuclear matrix associated protein; RAMP; Retinoic acid regulated nuclear matrix associated protein; Retinoic acid-regulated nuclear matrix-associated protein.
    纯化方法HPLC
    亚基Component of the DCX(DTL) E3 ubiquitin ligase complex, at least composed of CUL4 (CUL4A or CUL4B), DDB1, DTL/CDT2 and RBX1. Interacts with CDKN1A and CDT1.
    亚细胞定位Nucleus. Nucleus membrane; Peripheral membrane protein; Nucleoplasmic side. Cytoplasm, cytoskeleton, centrosome. Note=Nuclear matrix-associated protein. Translocates from the interphase nucleus to the metaphase cytoplasm during mitosis.
    组织特异性Expressed in placenta and testis, very low expression seen in skeletal muscle. Detected in all hematopoietic tissues examined, with highest expression in thymus and bone marrow. A low level detected in the spleen and lymph node, and barely detectable level in the peripheral leukocytes. RA treatment down-regulated the expression in NT2 cell.
    翻译后修饰Ubiquitinated by the anaphase promoting complex/cyclosome (APC/C).
    Phosphorylated upon DNA damage, probably by ATM or ATR.
    相似性Belongs to the WD repeat cdt2 family.
    Contains 7 WD repeats.
    功能Substrate-specific adapter of a DCX (DDB1-CUL4-X-box) E3 ubiquitin-protein ligase complex required for cell cycle control, DNA damage response and translesion DNA synthesis. The DCX(DTL) complex, also named CRL4(CDT2) complex, mediates the polyubiquitination and subsequent degradation of CDT1 and CDKN1A/p21(CIP1). CDT1 degradation in response to DNA damage is necessary to ensure proper cell cycle regulation of DNA replication. CDKN1A/p21(CIP1) degradation during S phase or following UV irradiation is essential to control replication licensing. Most substrates require their interaction with PCNA for their polyubiquitination: substrates interact with PCNA via their PIP-box, and those containing the 'K+4' motif in the PIP box, recruit the DCX(DTL) complex, leading to their degradation. In undamaged proliferating cells, the DCX(DTL) complex also promotes the 'Lys-164' monoubiquitination of PCNA, thereby being involved in PCNA-dependent translesion DNA synthesis.
    保存条件Shipped at 4℃. Stored at -20℃ for one year. Avoid repeated freeze/thaw cycles.
    注意事项This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
    背景资料Substrate-specific adapter of a DCX (DDB1-CUL4-X-box) E3 ubiquitin-protein ligase complex required for cell cycle control, DNA damage response and translesion DNA synthesis. The DCX(DTL) complex, also named CRL4(CDT2) complex, mediates the polyubiquitination and subsequent degradation of CDT1 and CDKN1A/p21(CIP1). CDT1 degradation in response to DNA damage is necessary to ensure proper cell cycle regulation of DNA replication. CDKN1A/p21(CIP1) degradation during S phase or following UV irradiation is essential to control replication licensing. Most substrates require their interaction with PCNA for their polyubiquitination: substrates interact with PCNA via their PIP-box, and those containing the 'K+4' motif in the PIP box, recruit the DCX(DTL) complex, leading to their degradation. In undamaged proliferating cells, the DCX(DTL) complex also promotes the 'Lys-164' monoubiquitination of PCNA, thereby being involved in PCNA-dependent translesion DNA synthesis.Tissue specificity: Expressed in placenta and testis, very low expression seen in skeletal muscle. Detected in all hematopoietic tissues examined, with highest expression in thymus and bone marrow. A low level detected in the spleen and lymph node, and barely detectable level in the peripheral leukocytes. RA treatment down-regulated the expression in NT2 cell.

     

     

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