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Plays a crucial role in cell survival and RAD51 foci formation in response to methylating DNA damage. Zusätzlich bieten wir Ihnen ATM Interactor Proteine (3) und und viele weitere Produktgruppen zu diesem Protein an.
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Cow (Bovine) Polyclonal ATMIN Primary Antibody für WB - ABIN2779685
Oka, Sakai, Sonoda, Nakamura, Asagoshi, Wilson, Kobayashi, Yamamoto, Heierhorst, Takeda, Taniguchi: DNA damage response protein ASCIZ links base excision repair with immunoglobulin gene conversion. in Biochemical and biophysical research communications 2008
WRNIP1 (zeige WRNIP1 Antikörper) connects PCNA (zeige PCNA Antikörper) monoubiquitination with ATMIN/ATM (zeige ATM Antikörper) to activate ATM (zeige ATM Antikörper) 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 (zeige TP53 Antikörper) and HIF-1alpha (zeige HIF1A Antikörper) in an oxygen dependent manner.
ATMIN is required for cell cycle progression and chromosome segregation following replication stress.ATMIN is required for the ATM (zeige ATM Antikörper)-mediated signaling and recruitment of 53BP1 (zeige TP53BP1 Antikörper) to DNA damage sites upon replication stress.
The ASCIZ-DYNLL1 (zeige DYNLL1 Antikörper) 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 (zeige DYNLL1 Antikörper) 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 (zeige RAD51 Antikörper) and ssDNA. ASCIZ foci depend on MLH1 (zeige MLH1 Antikörper).
ATMIN defines a novel NBS1 (zeige NBN Antikörper)-independent pathway of ATM (zeige ATM Antikörper) 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.
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 (zeige DYNLL1 Antikörper) are essential for the development and expansion of MYC (zeige MYC Antikörper)-driven B cell lymphoma.
These results reveal a new requirement for ATMIN-dependent ATM (zeige ATM Antikörper) signaling in TP53 (zeige TP53 Antikörper)-deficient glioblastoma multiforme, indicating a pro-tumorigenic role for ATM (zeige ATM Antikörper) 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 (zeige NBN Antikörper)
Results show that Atmin is critical for normal kidney development through Wnt (zeige WNT2 Antikörper) signaling pathway modifications.
ATMIN has a role in lung morphogenesis and ciliogenesis through transcriptional regulation
UBR5 (zeige UBR5 Antikörper)-mediated ATMIN ubiquitination is a vital event for ATM (zeige ATM Antikörper) pathway selection and activation in response to DNA damage
the antagonism and redundancy of ATMIN and NBS1 (zeige NBN Antikörper) constitute a crucial regulatory mechanism for ATM (zeige ATM Antikörper) signaling and function.
ASCIZ (ATMIN) regulates B cell development by inducing DYNLL1 (LC8 (zeige DYNLL1 Antikörper)) expression which in turn prevents Bim (zeige BCL2L11 Antikörper)-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