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Plays a crucial role in cell survival and RAD51 foci formation in response to methylating DNA damage. Additionally we are shipping ATM Interactor Proteins (3) and and many more products for this protein.
Showing 10 out of 37 products:
WRNIP1 (show WRNIP1 Antibodies) connects PCNA (show PCNA Antibodies) monoubiquitination with ATMIN/ATM (show ATM Antibodies) to activate ATM (show ATM Antibodies) 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 (show TP53 Antibodies) and HIF-1alpha (show HIF1A Antibodies) in an oxygen dependent manner.
ATMIN is required for cell cycle progression and chromosome segregation following replication stress.ATMIN is required for the ATM (show ATM Antibodies)-mediated signaling and recruitment of 53BP1 (show TP53BP1 Antibodies) to DNA damage sites upon replication stress.
The ASCIZ-DYNLL1 (show DYNLL1 Antibodies) 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 (show DYNLL1 Antibodies) 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 (show RAD51 Antibodies) and ssDNA. ASCIZ foci depend on MLH1 (show MLH1 Antibodies).
ATMIN defines a novel NBS1 (show NBN Antibodies)-independent pathway of ATM (show ATM Antibodies) 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 (show MYC Antibodies) expression, which is synthetic lethal with Dynll1 (show DYNLL1 Antibodies) deletion in B-2 cells, did not further reduce B-1a cell numbers in Dynll1 (show DYNLL1 Antibodies)-defcient mice. we found that the ASCIZ-DYNLL1 (show DYNLL1 Antibodies) axis was also required for the early-juvenile development of aggressive MYC (show MYC Antibodies)-driven and p53 (show TP53 Antibodies)-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 (show DYNLL1 Antibodies) are essential for the development and expansion of MYC (show MYC Antibodies)-driven B cell lymphoma.
These results reveal a new requirement for ATMIN-dependent ATM (show ATM Antibodies) signaling in TP53 (show TP53 Antibodies)-deficient glioblastoma multiforme, indicating a pro-tumorigenic role for ATM (show ATM Antibodies) 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 (show NBN Antibodies)
Results show that Atmin is critical for normal kidney development through Wnt (show WNT2 Antibodies) signaling pathway modifications.
ATMIN has a role in lung morphogenesis and ciliogenesis through transcriptional regulation
UBR5 (show UBR5 Antibodies)-mediated ATMIN ubiquitination is a vital event for ATM (show ATM Antibodies) pathway selection and activation in response to DNA damage
the antagonism and redundancy of ATMIN and NBS1 (show NBN Antibodies) constitute a crucial regulatory mechanism for ATM (show ATM Antibodies) signaling and function.
ASCIZ (ATMIN) regulates B cell development by inducing DYNLL1 (LC8 (show DYNLL1 Antibodies)) expression which in turn prevents Bim (show BCL2L11 Antibodies)-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