Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
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 (Montrer ATM Kits ELISA) mutations. ATM (Montrer ATM Kits ELISA) loss in other tumors also increases chromothripsis.
ASF1a (Montrer ASF1A Kits ELISA) promotes non-homologous end joining repair by facilitating phosphorylation of MDC1 (Montrer MDC1 Kits ELISA) by ATM (Montrer ATM Kits ELISA) 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 (Montrer ATM Kits ELISA) and ATG4C (Montrer ATG4C Kits ELISA) 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 (Montrer ATM Kits ELISA)-reactive oxygen species-iNOS (Montrer NOS2 Kits ELISA) axis regulates nitric oxide mediated cellular senescence.
DNA-PKcs (Montrer PRKDC Kits ELISA), which is integral to the non-homologous end joining pathway, negatively regulates ATM (Montrer ATM Kits ELISA) activity through phosphorylation of ATM (Montrer ATM Kits ELISA).
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 (Montrer ATM Kits ELISA)-dependent regulation of FOXO1 (Montrer FOXO1 Kits ELISA) 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 (Montrer ATM Kits ELISA)- and Rad-3-related (ATR (Montrer ANTXR1 Kits ELISA)) kinase activation in non-replicating cells is regulated by the XPB (Montrer GTF2H5 Kits ELISA) subunit of transcription factor IIH (TFIIH (Montrer GTF2H1 Kits ELISA))
variants in ATM (Montrer ATM Kits ELISA) 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 (Montrer CD44 Kits ELISA) in mouse and human PanIN lesions via activation of beta-catenin (Montrer CTNNB1 Kits ELISA) signaling, leading to the induction of an epithelial-to-mesenchymal transition (EMT (Montrer ITK Kits ELISA)) phenotype characterized by expression of Zeb1 (Montrer ZEB1 Kits ELISA) and Snail1 (Montrer SNAI1 Kits ELISA).
Histone deacetylase 9 (HDAC9 (Montrer HDAC9 Kits ELISA)) regulates the functions of the ATDC (TRIM29) protein
ATDC increases cell proliferation via inhibition of p53 (Montrer TP53 Kits ELISA) 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