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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 Antibodies (35) and and many more products for this protein.
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Repression of ATMIN in hypoxia is mediated by both p53 (show TP53 Proteins) and HIF-1alpha (show HIF1A Proteins) 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 Proteins)-mediated signaling and recruitment of 53BP1 (show TP53BP1 Proteins) to DNA damage sites upon replication stress.
The ASCIZ-DYNLL1 (show DYNLL1 Proteins) 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 Proteins) 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 Proteins) and ssDNA. ASCIZ foci depend on MLH1 (show MLH1 Proteins).
ATMIN defines a novel NBS1 (show NBN Proteins)-independent pathway of ATM (show ATM Proteins) 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.
ASCIZ (ATMIN) is structurally related to the yeast ATM (show ATM Proteins)/ATR (show ANTXR1 Proteins) substrate Mdt1 (show RDH11 Proteins) (Pin4 (show PIN4 Proteins)/Ybl051c); both proteins contain SQ/TQ cluster domains and interact with N-terminal FHA (show CRY2 Proteins) domains of CHK2/Rad53 (show CHEK2 Proteins) kinases.
ASCIZ and its target DYNLL1 (show DYNLL1 Proteins) are essential for the development and expansion of MYC (show MYC Proteins)-driven B cell lymphoma.
These results reveal a new requirement for ATMIN-dependent ATM (show ATM Proteins) signaling in TP53 (show TP53 Proteins)-deficient glioblastoma multiforme, indicating a pro-tumorigenic role for ATM (show ATM Proteins) 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 Proteins)
Results show that Atmin is critical for normal kidney development through Wnt (show WNT2 Proteins) signaling pathway modifications.
ATMIN has a role in lung morphogenesis and ciliogenesis through transcriptional regulation
UBR5-mediated ATMIN ubiquitination is a vital event for ATM (show ATM Proteins) pathway selection and activation in response to DNA damage
the antagonism and redundancy of ATMIN and NBS1 (show NBN Proteins) constitute a crucial regulatory mechanism for ATM (show ATM Proteins) signaling and function.
ASCIZ (ATMIN) regulates B cell development by inducing DYNLL1 (LC8 (show DYNLL1 Proteins)) expression which in turn prevents Bim (show BCL2L11 Proteins)-dependent apoptosis in immature B cells in the bone marrow
ATMIN has dual functions as an efficiency factor for DNA base damage repair as well as a key transcriptional regulator of early lung development.
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