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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Tumor protein p53 binding protein 1

53BP1, p53-binding protein 1
Top mentioned proteins: H2A, p53, Atm, Histone, Iris
Papers using 53BP1 antibodies
A Combinational Filtering Method for Enhancing Suspicious Structures in Chest X-rays
Anderson Rhona et al., In Genome Integrity, 2010
... Cells were then incubated with primary antibody (mouse monoclonal anti-human 53BP1 (BD Biosciences Clone 19) 1:200 in ...
Changes in the cell kinetics of pig epidermis after single doses of X rays.
Borgmann Kerstin, In PLoS ONE, 1987
... Rabbit anti-53BP1 NB100-304A31/300Acris-antibodies ...
Papers on 53BP1
Long-term exposure of A549 cells to titanium dioxide nanoparticles induces DNA damage and sensitizes cells towards genotoxic agents.
Carriere et al., Grenoble, France. In Nanotoxicology, Feb 2016
Genotoxic impact was assessed using alkaline and Fpg-modified comet assay, immunostaining of 53BP1 foci and the cytokinesis-blocked micronucleus assay.
RNF4 regulates DNA double-strand break repair in a cell cycle-dependent manner.
Ann et al., Duarte, United States. In Cell Cycle, Feb 2016
Notably, 53BP1 foci, but not BRCA1 foci, co-exist with pS824-KAP1 foci.
Radiation-induced loss of salivary gland function is driven by cellular senescence and prevented by IL-6 modulation.
Axelrod et al., In Cancer Res, Feb 2016
We demonstrate that the loss of salivary function was closely accompanied by cellular senescence, as evidenced by a persistent DNA damage response (γH2AX, 53BP1) and the expression of senescence-associated markers (SA-βgal, p19ARF, DcR2) and secretory phenotype (SASP) factors (PAI-1, IL-6).
TPP1 Blocks an ATR-Mediated Resection Mechanism at Telomeres.
de Lange et al., New York City, United States. In Mol Cell, Feb 2016
DSB resection is positively and negatively regulated by ATM signaling through CtIP/MRN and 53BP1-bound Rif1, respectively.
HELB Is a Feedback Inhibitor of DNA End Resection.
Durocher et al., Toronto, Canada. In Mol Cell, Feb 2016
HELB acts independently of 53BP1 and is exported from the nucleus as cells approach S phase, concomitant with the upregulation of resection.
Histone H1 couples initiation and amplification of ubiquitin signalling after DNA damage.
Mailand et al., Copenhagen, Denmark. In Nature, Dec 2015
Whereas RNF168 is known to catalyse ubiquitylation of H2A-type histones, leading to the recruitment of repair factors such as 53BP1 (refs 8-10), the critical substrates of RNF8 and K63-linked ubiquitylation remain elusive.
53BP1 and the LINC Complex Promote Microtubule-Dependent DSB Mobility and DNA Repair.
de Lange et al., New York City, United States. In Cell, Dec 2015
We find that the greater mobility of damaged chromatin requires 53BP1, SUN1/2 in the linker of the nucleoskeleton, and cytoskeleton (LINC) complex and dynamic microtubules.
DNA Damage Response Assessments in Human Tumor Samples Provide Functional Biomarkers of Radiosensitivity.
von Neubeck et al., Heidelberg, Germany. In Semin Radiat Oncol, Oct 2015
Investigators are increasingly studying the subnuclear accumulation (ie, foci) of proteins in the DNA damage response (DDR), such as gamma-H2AX, 53BP1, or RAD51, as a surrogate of treatment sensitivity.
Orientation-specific joining of AID-initiated DNA breaks promotes antibody class switching.
Alt et al., Boston, United States. In Nature, Oct 2015
We further implicate ATM-dependent DSB-response factors in enforcing this mechanism and provide an explanation of why CSR is so reliant on the 53BP1 DSB-response factor.
Biochemical mechanism of DSB end resection and its regulation.
Sung et al., New Haven, United States. In Dna Repair (amst), Aug 2015
Topics addressed will include how resection initiates via the introduction of an endonucleolytic incision close to the break end, the molecular mechanism of the conserved MRE11 complex in conjunction with Sae2/CtIP within such a model, the role of BRCA1 and 53BP1 in regulating resection initiation in mammalian cells, the influence of chromatin in the resection process, and potential roles of novel factors.
DNA damage foci: Meaning and significance.
Burdak-Rothkamm et al., United Kingdom. In Environ Mol Mutagen, Jul 2015
The discovery of DNA damage response proteins such as γH2AX, ATM, 53BP1, RAD51, and the MRE11/RAD50/NBS1 complex, that accumulate and/or are modified in the vicinity of a chromosomal DNA double-strand break to form microscopically visible, subnuclear foci, has revolutionized the detection of these lesions and has enabled studies of the cellular machinery that contributes to their repair.
REV7 counteracts DNA double-strand break resection and affects PARP inhibition.
Rottenberg et al., Amsterdam, Netherlands. In Nature, Jun 2015
REV7 is recruited to DSBs in a manner dependent on the H2AX-MDC1-RNF8-RNF168-53BP1 chromatin pathway, and seems to block HR and promote end joining in addition to its regulatory role in DNA damage tolerance.
Synthetic lethality in chronic lymphocytic leukaemia with DNA damage response defects by targeting the ATR pathway.
Stankovic et al., Waltham, United States. In Lancet, Mar 2015
In p53 or ATM defective cells, AZD6738 treatment resulted in replication fork stalls and accumulation of unrepaired DNA damage, as evidenced by γH2AX and 53BP1 foci formation, which was carried through into mitosis, resulting in cell death by mitotic catastrophe.
Double-strand break repair-adox: Restoration of suppressed double-strand break repair during mitosis induces genomic instability.
Shinohara et al., Ōsaka, Japan. In Cancer Sci, 2014
Cells have multiple safeguards to prevent genomic instability during mitosis: inhibition of 53BP1 or BRCA1 localization to DSB sites, which is important to promote non-homologous end joining or homologous recombination, respectively, and also modulation of the non-homologous end joining core complex to inhibit DSB repair.
Opinion: uracil DNA glycosylase (UNG) plays distinct and non-canonical roles in somatic hypermutation and class switch recombination.
Honjo et al., Kyoto, Japan. In Int Immunol, 2014
Interestingly, UNG has been associated with a CSR-specific repair adapter protein Brd4, which interacts with acetyl histone 4, γH2AX and 53BP1 to promote non-homologous end joining during CSR.
The role of ATM and 53BP1 as predictive markers in cervical cancer.
van Vugt et al., Groningen, Netherlands. In Int J Cancer, 2012
survival analysis revealed that ATM inhibition, but not 53BP1 depletion, strongly radiosensitised cervical cancer cells
Vaccinia-related kinase 1 (VRK1) is an upstream nucleosomal kinase required for the assembly of 53BP1 foci in response to ionizing radiation-induced DNA damage.
Lazo et al., Salamanca, Spain. In J Biol Chem, 2012
Data show that vaccinia-related kinase 1 (VRK1) in resting cells plays an important role in the formation of ionizing radiation-induced foci that assemble on the 53BP1 scaffold protein during the DNA damage response.
RNF8- and RNF168-dependent degradation of KDM4A/JMJD2A triggers 53BP1 recruitment to DNA damage sites.
Richard et al., Montréal, Canada. In Embo J, 2012
The authors propose that the RNF8-dependent degradation of JMJD2A regulates DNA repair by controlling the recruitment of 53BP1 at DNA damage sites.
53BP1 deficiency combined with telomere dysfunction activates ATR-dependent DNA damage response.
Blasco et al., Madrid, Spain. In J Cell Biol, 2012
deletion of 53BP1 in TRF1-deficient cells impairs the C-NHEJ repair pathway, decreasing the occurrence of chromosome-type end to end telomere fusions while inducing a persistent DNA damage signal that activates the ATR-dependent DDR and HR repair pathways
Overlapping functions between XLF repair protein and 53BP1 DNA damage response factor in end joining and lymphocyte development.
Zha et al., New York City, United States. In Proc Natl Acad Sci U S A, 2012
XLF repair protein and 53BP1 DNA damage response factor have overlapping functions in end joining and lymphocyte development
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