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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 et et beaucoup plus de produits pour cette protéine.
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Cow (Bovine) Polyclonal ATMIN Primary Antibody pour 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. dans Biochemical and biophysical research communications 2008
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.
ASCIZ (ATMIN) is structurally related to the yeast ATM (Montrer ATM Anticorps)/ATR (Montrer ANTXR1 Anticorps) substrate Mdt1 (Montrer RDH11 Anticorps) (Pin4 (Montrer PIN4 Anticorps)/Ybl051c); both proteins contain SQ/TQ cluster domains and interact with N-terminal FHA (Montrer CRY2 Anticorps) domains of CHK2/Rad53 (Montrer CHEK2 Anticorps) kinases.
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
ATMIN has dual functions as an efficiency factor for DNA base damage repair as well as a key transcriptional regulator of early lung development.
Identify a role for ATMIN in regulating the maintenance of genomic stability and tumor suppression in B cells.
Asciz is essential for mouse embryonic development and lung organogenesis likely as a transcription factor
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