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Plays a crucial role in cell survival and RAD51 foci formation in response to methylating DNA damage. De plus, nous expédions ATM Interactor Protéines (3) et et beaucoup plus de produits pour cette protéine.
Showing 10 out of 37 products:
WRNIP1 (Montrer WRNIP1 Anticorps) connects PCNA (Montrer PCNA Anticorps) monoubiquitination with ATMIN/ATM (Montrer ATM Anticorps) to activate ATM (Montrer ATM Anticorps) signalling in response to replication stress and contribute to the maintenance of genomic stability.
Studies suggest that ATM INteractor (ATMIN) could be an important biomarker in disease prognosis and treatment that might lighten the burden of chronic kidney disease and also affect on its progression.
Repression of ATMIN in hypoxia is mediated by both p53 (Montrer TP53 Anticorps) and HIF-1alpha (Montrer HIF1A Anticorps) in an oxygen dependent manner.
ATMIN is required for cell cycle progression and chromosome segregation following replication stress.ATMIN is required for the ATM (Montrer ATM Anticorps)-mediated signaling and recruitment of 53BP1 (Montrer TP53BP1 Anticorps) to DNA damage sites upon replication stress.
The ASCIZ-DYNLL1 (Montrer DYNLL1 Anticorps) feedback loop represents a novel mechanism for auto-regulation of gene expression, where the gene product directly inhibits the transcriptional activator while bound at its own promoter.
these results imply a potential cellular interference between DYNLL1 (Montrer DYNLL1 Anticorps) and ATMIN functions.
Asciz (Atmin) deletion or knock-down does not affect ATM levels and activation in mouse, chicken, or human cells
ATM/ATR-Substrate Chk2-Interacting Zn2+-finger protein (ASCIZ) required for repair of abasic sites after methylating and oxidative DNA damage but not double-strand breaks. Forms DNA damage-induced foci with RAD51 (Montrer RAD51 Anticorps) and ssDNA. ASCIZ foci depend on MLH1 (Montrer MLH1 Anticorps).
ATMIN defines a novel NBS1 (Montrer NBN Anticorps)-independent pathway of ATM (Montrer ATM Anticorps) signalling.
These data suggest that ASCIZ may affect the choice between competing base repair pathways in a manner that reduces the amount of substrates available for Ig gene conversion.
oncogenic MYC (Montrer MYC Anticorps) expression, which is synthetic lethal with Dynll1 (Montrer DYNLL1 Anticorps) deletion in B-2 cells, did not further reduce B-1a cell numbers in Dynll1 (Montrer DYNLL1 Anticorps)-defcient mice. we found that the ASCIZ-DYNLL1 (Montrer DYNLL1 Anticorps) axis was also required for the early-juvenile development of aggressive MYC (Montrer MYC Anticorps)-driven and p53 (Montrer TP53 Anticorps)-deficient B cell lymphomas.
ATMIN, therefore, has multiple roles in different cell types, and its absence results in perturbed hematopoiesis, especially during stress conditions and aging.
ASCIZ and its target DYNLL1 (Montrer DYNLL1 Anticorps) are essential for the development and expansion of MYC (Montrer MYC Anticorps)-driven B cell lymphoma.
These results reveal a new requirement for ATMIN-dependent ATM (Montrer ATM Anticorps) signaling in TP53 (Montrer TP53 Anticorps)-deficient glioblastoma multiforme, indicating a pro-tumorigenic role for ATM (Montrer ATM Anticorps) in the context of these tumors.
findings reveal a novel model for an intestinal bowel disease phenotype that occurs upon combined loss of the DNA repair cofactors ATMIN and NBS1 (Montrer NBN Anticorps)
Results show that Atmin is critical for normal kidney development through Wnt (Montrer WNT2 Anticorps) signaling pathway modifications.
ATMIN has a role in lung morphogenesis and ciliogenesis through transcriptional regulation
UBR5 (Montrer UBR5 Anticorps)-mediated ATMIN ubiquitination is a vital event for ATM (Montrer ATM Anticorps) pathway selection and activation in response to DNA damage
the antagonism and redundancy of ATMIN and NBS1 (Montrer NBN Anticorps) constitute a crucial regulatory mechanism for ATM (Montrer ATM Anticorps) signaling and function.
ASCIZ (ATMIN) regulates B cell development by inducing DYNLL1 (LC8 (Montrer DYNLL1 Anticorps)) expression which in turn prevents Bim (Montrer BCL2L11 Anticorps)-dependent apoptosis in immature B cells in the bone marrow
Plays a crucial role in cell survival and RAD51 foci formation in response to methylating DNA damage. Involved in regulating the activity of ATM in the absence of DNA damage. May play a role in stabilizing ATM.
, ATM INteracting protein
, ATM/ATR-Substrate Chk2-Interacting Zn++-finger protein
, ATM/ATR-substrate CHEK2-interacting zinc finger protein
, ATM/ATR-substrate CHK2-interacting zinc finger protein
, zinc finger protein 822
, ATM/ATR-Substrate Chk2-Interacting Zn2+-finger protein