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Correction to: KAP1 modulates osteogenic diferentiation via the ERK/Runx2 cascade in vascular smooth muscle cells.
Mol Biol Rep
September 2023
Department of Nephrology, The Fourth Hospital of Hebei Medical University, Hebei Clinical Research Center for Chronic Kidney Disease, Hebei Key Laboratory of Vascular Calcifcation in Kidney Disease, Shijiazhuang, P.R. China.
Correction to: KAP1 modulates osteogenic differentiation via the ERK/Runx2 cascade in vascular smooth muscle cells.
Mol Biol Rep
July 2023
Department of Nephrology, The Fourth Hospital of Hebei Medical University, Hebei Clinical Research Center for Chronic Kidney Disease, Hebei Key Laboratory of Vascular Calcification in Kidney Disease, Shijiazhuang, P. R. China.
KAP1 is a new non-genetic vulnerability of malignant pleural mesothelioma (MPM).
NAR Cancer
September 2022
Laboratory of Translational Research, Azienda USL-IRCCS di Reggio Emilia, 42123 Reggio Emilia, Italy.
Malignant pleural mesothelioma (MPM) is a rare and incurable cancer, which incidence is increasing in many countries. MPM escapes the classical genetic model of cancer evolution, lacking a distinctive genetic fingerprint. Omics profiling revealed extensive heterogeneity failing to identify major vulnerabilities and restraining development of MPM-oriented therapies.
View Article and Find Full Text PDFCorrection of ATM mutations in iPS cells from two ataxia-telangiectasia patients restores DNA damage and oxidative stress responses.
Hum Mol Genet
April 2020
Australian Institute for Bioengineering and Nanotechnology (AIBN), The University of Queensland, St. Lucia, Brisbane, QLD 4072, Australia.
Patients with ataxia-telangiectasia (A-T) lack a functional ATM kinase protein and exhibit defective repair of DNA double-stranded breaks and response to oxidative stress. We show that CRISPR/Cas9-assisted gene correction combined with piggyBac (PB) transposon-mediated excision of the selection cassette enables seamless restoration of functional ATM alleles in induced pluripotent stem cells from an A-T patient carrying compound heterozygous exonic missense/frameshift mutations, and from a patient with a homozygous splicing acceptor mutation of an internal coding exon. We show that the correction of one allele restores expression of ~ 50% of full-length ATM protein and ameliorates DNA damage-induced activation (auto-phosphorylation) of ATM and phosphorylation of its downstream targets, KAP-1 and H2AX.
View Article and Find Full Text PDFCorrection for Gjyshi et al., "Activated Nrf2 Interacts with Kaposi's Sarcoma-Associated Herpesvirus Latency Protein LANA-1 and Host Protein KAP1 To Mediate Global Lytic Gene Repression".
J Virol
December 2017
H. M. Bligh Cancer Research Laboratories, Department of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
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