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anti-Human TRIM29 Antibodies:
anti-Mouse (Murine) TRIM29 Antibodies:
anti-Rat (Rattus) TRIM29 Antibodies:
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Human Polyclonal TRIM29 Primary Antibody for ELISA, IHC - ABIN4362410
Kosaka, Inoue, Ohmachi, Yokoe, Matsumoto, Mimori, Tanaka, Watanabe, Mori: Tripartite motif-containing 29 (TRIM29) is a novel marker for lymph node metastasis in gastric cancer. in Annals of surgical oncology 2007
Human Polyclonal TRIM29 Primary Antibody for ELISA, IHC - ABIN4362411
Wang, Heidt, Lee, Yang, Logsdon, Zhang, Fearon, Ljungman, Simeone: Oncogenic function of ATDC in pancreatic cancer through Wnt pathway activation and beta-catenin stabilization. in Cancer cell 2009
Human Polyclonal TRIM29 Primary Antibody for IHC (fro), ELISA - ABIN537436
Katkoori, Shanmugam, Jia, Vitta, Sthanam, Callens, Messiaen, Chen, Zhang, Bumpers, Samuel, Manne: Prognostic significance and gene expression profiles of p53 mutations in microsatellite-stable stage III colorectal adenocarcinomas. in PLoS ONE 2012
ASF1a (show ASF1A Antibodies) promotes non-homologous end joining repair by facilitating phosphorylation of MDC1 (show MDC1 Antibodies) by ATM (show ATM Antibodies) at double-strand breaks.
ectopic expression of Gene 33 triggers DNA damage response in an ATM serine/threonine kinase (ATM)-dependent fashion and through pathways dependent or not dependent on ABL proto-oncogene 1 non-receptor tyrosine kinase (c-Abl).
We demonstrate that, in breast cancer cells, ATM (show ATM Antibodies) and ATG4C (show ATG4C Antibodies) are essential drivers of mammosphere formation, suggesting that their targeting may improve current approaches to eradicate breast cancer cells with a stem-like phenotype.
ATM (show ATM Antibodies)-reactive oxygen species-iNOS (show NOS2 Antibodies) axis regulates nitric oxide mediated cellular senescence.
DNA-PKcs (show PRKDC Antibodies), which is integral to the non-homologous end joining pathway, negatively regulates ATM (show ATM Antibodies) activity through phosphorylation of ATM (show ATM Antibodies).
The data suggest that pre-B cells are endowed with a protective mechanism that reduces the risk for aberrant recombinations and chromosomal translocations when exposed to DNA damage, involving the ATM (show ATM Antibodies)-dependent regulation of FOXO1 (show FOXO1 Antibodies) binding to the Erag enhancer region.
Data suggest HSP90AA1-dependent regulation of ATM-NBN-CHK2 and ATR-CHK1 axes influences cells capability to repair double-stranded DNA damage; mechanisms include phosphorylation, polyubiquitination, and proteasomal degradation/proteolysis. (HSP90AA1 = heat shock protein 90kDa alpha; ATM = ataxia telangiectasia mutated protein; NBN = nibrin; CHK = checkpoint kinase; ATR = ataxia telangiectasia and Rad3 related kinase)
DNA damage-induced ATM (show ATM Antibodies)- and Rad (show RRAD Antibodies)-3-related (ATR (show ANTXR1 Antibodies)) kinase activation in non-replicating cells is regulated by the XPB (show GTF2H5 Antibodies) subunit of transcription factor IIH (TFIIH (show GTF2H1 Antibodies))
variants in ATM (show ATM Antibodies) were associated with moderate risks of breast cancer.
We report that endogenous huntingtin (show HTT Antibodies) protein directly participates in oxidative DNA damage repair. Using novel chromobodies to detect endogenous human huntingtin (show HTT Antibodies) in live cells, we show that localization of huntingtin (show HTT Antibodies) to DNA damage sites is dependent on the kinase activity of ataxia telangiectasia mutated (ATM (show ATM Antibodies)) protein.
this study shows that deletion of TRIM29 enhanced macrophage production of type I interferons and protected mice from infection with influenza virus, while challenge of Trim29-/- mice with Haemophilus influenzae resulted in lethal lung inflammation due to massive production of proinflammatory cytokines by macrophages
Findings established a role for ATDC/TRIM29 as a robust pathogenic driver of bladder cancer development, identified downstream effector pathways, and implicated ATDC as a candidate biomarker and therapeutic target.
ATDC up-regulates CD44 (show CD44 Antibodies) in mouse and human PanIN lesions via activation of beta-catenin (show CTNNB1 Antibodies) signaling, leading to the induction of an epithelial-to-mesenchymal transition (EMT (show ITK Antibodies)) phenotype characterized by expression of Zeb1 (show ZEB1 Antibodies) and Snail1 (show SNAI1 Antibodies).
Histone deacetylase 9 (HDAC9 (show HDAC9 Antibodies)) regulates the functions of the ATDC (TRIM29) protein
ATDC increases cell proliferation via inhibition of p53 (show TP53 Antibodies) nuclear activities.
The protein encoded by this gene belongs to the TRIM protein family. It has multiple zinc finger motifs and a leucine zipper motif. It has been proposed to form homo- or heterodimers which are involved in nucleic acid binding. Thus, it may act as a transcriptional regulatory factor involved in carcinogenesis and/or differentiation. It may also function in the suppression of radiosensitivity since it is associated with ataxia telangiectasia phenotype.
tripartite motif-containing 29
, tripartite motif protein TRIM29
, tripartite motif-containing protein 29-like
, A-T mutated
, AT mutated
, TEL1, telomere maintenance 1, homolog
, serine-protein kinase ATM
, ataxia telangiectasia group D-associated protein
, ataxia-telangiectasia group D-associated protein
, tripartite motif-containing protein 29
, tripartite motif protein 29