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A high frequency of chromothriptic events occurred in cases of acute lymphoblastic anemia arising in patients with ataxia telangectasia, specifically on acrocentric chromosomes, as compared with tumors from individuals with other types of DNA repair syndromes, due to the short telomeres and poor DNA repair caused by their two ATM (show ATM Proteins) mutations. ATM (show ATM Proteins) loss in other tumors also increases chromothripsis.
ASF1a (show ASF1A Proteins) promotes non-homologous end joining repair by facilitating phosphorylation of MDC1 by ATM (show ATM Proteins) 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 Proteins) and ATG4C (show ATG4C Proteins) 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 Proteins)-reactive oxygen species-iNOS (show NOS2 Proteins) axis regulates nitric oxide mediated cellular senescence.
DNA-PKcs (show PRKDC Proteins), which is integral to the non-homologous end joining pathway, negatively regulates ATM (show ATM Proteins) activity through phosphorylation of ATM (show ATM Proteins).
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 Proteins)-dependent regulation of FOXO1 (show FOXO1 Proteins) 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 Proteins)- and Rad-3-related (ATR (show ANTXR1 Proteins)) kinase activation in non-replicating cells is regulated by the XPB (show GTF2H5 Proteins) subunit of transcription factor IIH (TFIIH (show GTF2H1 Proteins))
variants in ATM (show ATM Proteins) were associated with moderate risks of breast cancer.
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 Proteins) in mouse and human PanIN lesions via activation of beta-catenin (show CTNNB1 Proteins) signaling, leading to the induction of an epithelial-to-mesenchymal transition (EMT (show ITK Proteins)) phenotype characterized by expression of Zeb1 and Snail1 (show SNAI1 Proteins).
Histone deacetylase 9 (HDAC9 (show HDAC9 Proteins)) regulates the functions of the ATDC (TRIM29) protein
ATDC increases cell proliferation via inhibition of p53 (show TP53 Proteins) 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