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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 (zeige ATM ELISA Kits) mutations. ATM (zeige ATM ELISA Kits) loss in other tumors also increases chromothripsis.
ASF1a (zeige ASF1A ELISA Kits) promotes non-homologous end joining repair by facilitating phosphorylation of MDC1 (zeige MDC1 ELISA Kits) by ATM (zeige ATM ELISA Kits) 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 (zeige ATM ELISA Kits) and ATG4C (zeige ATG4C ELISA Kits) 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 (zeige ATM ELISA Kits)-reactive oxygen species-iNOS (zeige NOS2 ELISA Kits) axis regulates nitric oxide mediated cellular senescence.
DNA-PKcs (zeige PRKDC ELISA Kits), which is integral to the non-homologous end joining pathway, negatively regulates ATM (zeige ATM ELISA Kits) activity through phosphorylation of ATM (zeige ATM ELISA Kits).
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 (zeige ATM ELISA Kits)-dependent regulation of FOXO1 (zeige FOXO1 ELISA Kits) 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 (zeige ATM ELISA Kits)- and Rad-3-related (ATR (zeige ANTXR1 ELISA Kits)) kinase activation in non-replicating cells is regulated by the XPB (zeige GTF2H5 ELISA Kits) subunit of transcription factor IIH (TFIIH (zeige GTF2H1 ELISA Kits))
variants in ATM (zeige ATM ELISA Kits) 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 (zeige CD44 ELISA Kits) in mouse and human PanIN lesions via activation of beta-catenin (zeige CTNNB1 ELISA Kits) signaling, leading to the induction of an epithelial-to-mesenchymal transition (EMT (zeige ITK ELISA Kits)) phenotype characterized by expression of Zeb1 (zeige ZEB1 ELISA Kits) and Snail1 (zeige SNAI1 ELISA Kits).
Histone deacetylase 9 (HDAC9 (zeige HDAC9 ELISA Kits)) regulates the functions of the ATDC (TRIM29) protein
ATDC increases cell proliferation via inhibition of p53 (zeige TP53 ELISA Kits) 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