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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. Additionally we are shipping DTL Antibodies (49) and DTL Proteins (3) and many more products for this protein.
Findings suggest that DTL (show TNFSF13B ELISA Kits) overexpression plays a crucial role in tumor cell proliferation in gastric carcinoma.
CDT2 mediated XPG (show ERCC5 ELISA Kits) elimination from DNA damage sites clears the chromatin space needed for repair.
CDT2 likely is a non-oncogene (show RAB1A ELISA Kits) to which transformed cells become addicted because of their enhanced cellular stress, such as replicative stress and DNA damage.
These findings reveal C/EBPalpha (show CEBPA ELISA Kits) regulates G1/S cell cycle arrest in response to DNA damage via the control of CRL4(Cdt2) mediated degradation of p21 (show CDKN1A ELISA Kits).
CDK1 activity blocks CRL4CDT2 by preventing chromatin recruitment of the substrate receptor, CDT2.
while interaction with PCNA (show PCNA ELISA Kits) was important for targeting p21 (show CDKN1A ELISA Kits) to the CRL4Cdt2 ligase re-localized to MVM replication centers
CRL4(Cdt2)-dependent degradation of TDG (show TDG ELISA Kits) occurs in S phase because of the requirement for TDG (show TDG ELISA Kits) to interact with chromatin-loaded PCNA (show PCNA ELISA Kits), and this degradation is important for preventing toxicity from excess TDG (show TDG ELISA Kits).
Data shows that phosphorylation of Cdt2 at T464 is important fot its interaction with Cdt2.
TGF-beta signaling promotes exit from the cell cycle and cellular migration through cullin cross-regulation: SCF-FBXO11 turns off CRL4-Cdt2.
ubiquitination of p12 through CRL4(Cdt2) and subsequent degradation form one mechanism by which a cell responds to DNA damage to inhibit fork progression.
while interaction with PCNA (show PCNA ELISA Kits) was important for targeting p21 to the CRL4Cdt2 ligase re-localized to MVM replication centers
L2dtl gene expression is essential for very early mouse embryonic development
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 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 (By similarity).
DDB1 and CUL4 associated factor 2
, DDB1- and CUL4-associated factor 2
, RA regulated nuclear matrix associated protein
, RA-regulated nuclear matrix-associated protein
, denticleless homolog
, denticleless protein homolog
, lethal(2) denticleless protein homolog
, retinoic acid-regulated nuclear matrix-associated protein
, Meth A ramp
, meth A retinoic acid-regulated nuclear matrix-associated protein
, retinoic-acid regulated nuclear matrix-associated protein