Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping activities during chromosomal signal joint formation.
about
Functional redundancy between the XLF and DNA-PKcs DNA repair factors in V(D)J recombination and nonhomologous DNA end joiningXRCC4's interaction with XLF is required for coding (but not signal) end joiningThe response to and repair of RAG-mediated DNA double-strand breaksFunctional intersection of ATM and DNA-dependent protein kinase catalytic subunit in coding end joining during V(D)J recombinationApurinic/apyrimidinic endonuclease 2 regulates the expansion of germinal centers by protecting against activation-induced cytidine deaminase-independent DNA damage in B cells.Methotrexate inhibits NF-κB activity via long intergenic (noncoding) RNA-p21 inductionUnique and redundant functions of ATM and DNA-PKcs during V(D)J recombinationDifferential phosphorylation of DNA-PKcs regulates the interplay between end-processing and end-ligation during nonhomologous end-joining.All stressed out without ATM kinaseOverlapping functions between XLF repair protein and 53BP1 DNA damage response factor in end joining and lymphocyte developmentKinase-dead ATM protein causes genomic instability and early embryonic lethality in miceIntegrated signaling in developing lymphocytes: the role of DNA damage responses.Restoration of ATM Expression in DNA-PKcs-Deficient Cells Inhibits Signal End Joining.Lymphocyte development: integration of DNA damage response signaling.Non-homologous end joining repair in Xenopus egg extractFunctional overlaps between XLF and the ATM-dependent DNA double strand break response.Kruppel-associated box (KRAB) proteins in the adaptive immune system.Programmed DNA breaks in lymphoid cells: repair mechanisms and consequences in human diseaseRepair of chromosomal RAG-mediated DNA breaks by mutant RAG proteins lacking phosphatidylinositol 3-like kinase consensus phosphorylation sites.TDP1 promotes assembly of non-homologous end joining protein complexes on DNA.Deficiency of XLF and PAXX prevents DNA double-strand break repair by non-homologous end joining in lymphocytes.CC-115, a dual inhibitor of mTOR kinase and DNA-PK, blocks DNA damage repair pathways and selectively inhibits ATM-deficient cell growth in vitro.Synthetic lethality between murine DNA repair factors XLF and DNA-PKcs is rescued by inactivation of Ku70.RNA-binding protein RBM14 regulates dissociation and association of non-homologous end joining proteins.
P2860
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P2860
Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping activities during chromosomal signal joint formation.
description
2011 nî lūn-bûn
@nan
2011 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Ataxia telangiectasia mutated ...... osomal signal joint formation.
@ast
Ataxia telangiectasia mutated ...... osomal signal joint formation.
@en
type
label
Ataxia telangiectasia mutated ...... osomal signal joint formation.
@ast
Ataxia telangiectasia mutated ...... osomal signal joint formation.
@en
prefLabel
Ataxia telangiectasia mutated ...... osomal signal joint formation.
@ast
Ataxia telangiectasia mutated ...... osomal signal joint formation.
@en
P2093
P2860
P356
P1476
Ataxia telangiectasia mutated ...... osomal signal joint formation.
@en
P2093
Andre Nussenzweig
Andrea Bredemeyer
Barry P Sleckman
Craig H Bassing
Elsa Callen
Eric J Gapud
Grace K Mahowald
Jeffrey J Bednarski
Kazuo Q Omi
P2860
P304
P356
10.1073/PNAS.1013295108
P407
P577
2011-01-18T00:00:00Z