Pages that link to "Q24649590"
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The following pages link to Essential role for DNA-PKcs in DNA double-strand break repair and apoptosis in ATM-deficient lymphocytes (Q24649590):
Displaying 50 items.
- ATM damage response and XLF repair factor are functionally redundant in joining DNA breaks (Q24596775) (← links)
- Functional redundancy between the XLF and DNA-PKcs DNA repair factors in V(D)J recombination and nonhomologous DNA end joining (Q24624166) (← links)
- Modeling the study of DNA damage responses in mice (Q26826949) (← links)
- Related Mechanisms of Antibody Somatic Hypermutation and Class Switch Recombination (Q27000758) (← links)
- The response to and repair of RAG-mediated DNA double-strand breaks (Q28256889) (← links)
- ATM Limits Incorrect End Utilization during Non-Homologous End Joining of Multiple Chromosome Breaks (Q28476006) (← links)
- Functional intersection of ATM and DNA-dependent protein kinase catalytic subunit in coding end joining during V(D)J recombination (Q28508673) (← links)
- Mechanism of suppression of chromosomal instability by DNA polymerase POLQ (Q28543483) (← links)
- Rif1 prevents resection of DNA breaks and promotes immunoglobulin class switching (Q29465549) (← links)
- Investigation of the functional link between ATM and NBS1 in the DNA damage response in the mouse cerebellum (Q30499891) (← links)
- A novel mouse model for ataxia-telangiectasia with a N-terminal mutation displays a behavioral defect and a low incidence of lymphoma but no increased oxidative burden (Q30806557) (← links)
- Inositol pyrophosphates mediate the DNA-PK/ATM-p53 cell death pathway by regulating CK2 phosphorylation of Tti1/Tel2 (Q33570316) (← links)
- A type I IFN-dependent DNA damage response regulates the genetic program and inflammasome activation in macrophages (Q33617275) (← links)
- Alternative end-joining catalyzes class switch recombination in the absence of both Ku70 and DNA ligase 4. (Q33656097) (← links)
- Alternative end-joining catalyzes robust IgH locus deletions and translocations in the combined absence of ligase 4 and Ku70 (Q33733981) (← links)
- Analysis of DNA polymerase ν function in meiotic recombination, immunoglobulin class-switching, and DNA damage tolerance. (Q33803398) (← links)
- Transcription-dependent activation of ataxia telangiectasia mutated prevents DNA-dependent protein kinase-mediated cell death in response to topoisomerase I poison (Q33832626) (← links)
- Origin of chromosomal translocations in lymphoid cancer (Q33870612) (← links)
- HIV-1 causes CD4 cell death through DNA-dependent protein kinase during viral integration. (Q34348888) (← links)
- DNA double-strand break signaling and human disorders (Q34360500) (← links)
- Loss of ATM kinase activity leads to embryonic lethality in mice (Q34368454) (← links)
- Ataxia telangiectasia-mutated protein and DNA-dependent protein kinase have complementary V(D)J recombination functions (Q34549990) (← links)
- Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping activities during chromosomal signal joint formation (Q34550115) (← links)
- The catalytic subunit of DNA-dependent protein kinase is required for cellular resistance to oxidative stress independent of DNA double-strand break repair. (Q34707456) (← links)
- Congenital bone marrow failure in DNA-PKcs mutant mice associated with deficiencies in DNA repair (Q34825234) (← links)
- Can the DNA damage response be harnessed to modulate atherosclerotic plaque phenotype? (Q35141697) (← links)
- Unique and redundant functions of ATM and DNA-PKcs during V(D)J recombination (Q35159001) (← links)
- Docosahexaenoic acid (DHA) sensitizes brain tumor cells to etoposide-induced apoptosis (Q35510360) (← links)
- Differential phosphorylation of DNA-PKcs regulates the interplay between end-processing and end-ligation during nonhomologous end-joining (Q35555378) (← links)
- Overlapping functions between XLF repair protein and 53BP1 DNA damage response factor in end joining and lymphocyte development (Q35844884) (← links)
- Interaction of cellular proteins with BCL-xL targeted to cytoplasmic inclusion bodies in adenovirus infected cells (Q35893900) (← links)
- H2AX phosphorylation at the sites of DNA double-strand breaks in cultivated mammalian cells and tissues (Q36001923) (← links)
- Disease severity in a mouse model of ataxia telangiectasia is modulated by the DNA damage checkpoint gene Hus1 (Q36083139) (← links)
- Kinase-dead ATM protein causes genomic instability and early embryonic lethality in mice (Q36145724) (← links)
- Enhanced cytotoxicity of PARP inhibition in mantle cell lymphoma harbouring mutations in both ATM and p53 (Q36238650) (← links)
- DEK is required for homologous recombination repair of DNA breaks (Q36314320) (← links)
- Non-redundant Functions of ATM and DNA-PKcs in Response to DNA Double-Strand Breaks. (Q36349861) (← links)
- DAB2IP regulates autophagy in prostate cancer in response to combined treatment of radiation and a DNA-PKcs inhibitor (Q36520723) (← links)
- ILKAP, ILK and PINCH1 control cell survival of p53-wildtype glioblastoma cells after irradiation (Q36544158) (← links)
- Potential of Radiation-Induced Cellular Stress for Reactivation of Latent HIV-1 and Killing of Infected Cells (Q36601890) (← links)
- The ATR barrier to replication-born DNA damage. (Q36664049) (← links)
- DNA-PKcs controls an endosomal signaling pathway for a proinflammatory response by natural killer cells (Q36691800) (← links)
- The ATM signaling network in development and disease (Q36712849) (← links)
- Lymphocyte development: integration of DNA damage response signaling (Q36846366) (← links)
- The ATM substrate KAP1 controls DNA repair in heterochromatin: regulation by HP1 proteins and serine 473/824 phosphorylation (Q36972711) (← links)
- Non-homologous end joining repair in Xenopus egg extract (Q37024061) (← links)
- A Damage-Independent Role for 53BP1 that Impacts Break Order and Igh Architecture during Class Switch Recombination (Q37052916) (← links)
- ATM deficiency sensitizes mantle cell lymphoma cells to poly(ADP-ribose) polymerase-1 inhibitors (Q37059580) (← links)
- Kinase-dead ATM protein is highly oncogenic and can be preferentially targeted by Topo-isomerase I inhibitors (Q37119667) (← links)
- Induction and inhibition of the pan-nuclear gamma-H2AX response in resting human peripheral blood lymphocytes after X-ray irradiation (Q37164350) (← links)