中文名稱：DTL 抗原（重組蛋白）

英文名稱：DTL Antigen (Recombinant Protein)

別名：denticleless E3 ubiquitin protein ligase homolog; CDT2; RAMP; DCAF2; L2DTL

儲存：冷凍（-20℃）

相關類別：抗原

概述

Fusion protein corresponding to a region derived from 531-730 amino acids of human DTL

技術規格

Full name:

denticleless E3 ubiquitin protein ligase homolog

Synonyms:

CDT2; RAMP; DCAF2; L2DTL

Swissprot:

Q9NZJ0

Gene Accession:

BC033540

Purity:

>85%, as determined by Coomassie blue stained SDS-PAGE

Expression system:

Escherichia coli

Tags:

His tag C-Terminus, GST tag N-Terminus

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, CDKN1A/p21(CIP1), FBXO18/FBH1 and KMT5A (PubMed:16861906, PubMed:16949367, PubMed:16964240, PubMed:17085480, PubMed:18703516, PubMed:18794347, PubMed:18794348, PubMed:19332548, PubMed:20129063, PubMed:23478441, PubMed:23478445, PubMed:23677613). CDT1 degradation in response to DNA damage is necessary to ensure proper cell cycle regulation of DNA replication (PubMed:16861906, PubMed:16949367, PubMed:17085480). CDKN1A/p21(CIP1) degradation during S phase or following UV irradiation is essential to control replication licensing (PubMed:18794348, PubMed:19332548). KMT5A degradation is also important for a proper regulation of mechanisms such as TGF-beta signaling, cell cycle progression, DNA repair and cell migration (PubMed:23478445). 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 (PubMed:20129063, PubMed:23478441, PubMed:23478445, PubMed:23677613).

展開全部

DTL 抗原（重組蛋白）說明書
下載

久久综合九九-久久综合九九亚洲一区-久久综合九色-久久综合九色欧美综合狠狠-久久综合九色婷婷97-久久综合九色综合8888

021-54845833/15800441009

ELISA試劑盒

PCR試劑盒

生化試劑盒

細胞系

細胞庫

基礎培養基

完全培養基

原代細胞

細胞專用培養基

菌株

生化試劑

病理染色液

科研抗體

標準品

血清

產品中心

最新產品

相關文章

DTL 抗原（重組蛋白）

Full name:	denticleless E3 ubiquitin protein ligase homolog
Synonyms:	CDT2; RAMP; DCAF2; L2DTL
Swissprot:	Q9NZJ0
Gene Accession:	BC033540
Purity:	>85%, as determined by Coomassie blue stained SDS-PAGE
Expression system:	Escherichia coli
Tags:	His tag C-Terminus, GST tag N-Terminus
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, CDKN1A/p21(CIP1), FBXO18/FBH1 and KMT5A (PubMed:16861906, PubMed:16949367, PubMed:16964240, PubMed:17085480, PubMed:18703516, PubMed:18794347, PubMed:18794348, PubMed:19332548, PubMed:20129063, PubMed:23478441, PubMed:23478445, PubMed:23677613). CDT1 degradation in response to DNA damage is necessary to ensure proper cell cycle regulation of DNA replication (PubMed:16861906, PubMed:16949367, PubMed:17085480). CDKN1A/p21(CIP1) degradation during S phase or following UV irradiation is essential to control replication licensing (PubMed:18794348, PubMed:19332548). KMT5A degradation is also important for a proper regulation of mechanisms such as TGF-beta signaling, cell cycle progression, DNA repair and cell migration (PubMed:23478445). 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 (PubMed:20129063, PubMed:23478441, PubMed:23478445, PubMed:23677613).