资料摘要
资料下载维甲酸调节核基质相关蛋白抗体 Background: 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. Also known as: 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.维甲酸调节核基质相关蛋白抗体
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