MABE1084

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Showing 1-15 of 15 results for "MABE1084" within Papers

Isolation and detection of DNA-protein crosslinks in mammalian cells.

Ignacio Torrecilla et al.

Nucleic acids research, 52(2), 525-547 (2023-12-12)

DNA-protein crosslinks (DPCs) are toxic DNA lesions wherein a protein is covalently attached to DNA. If not rapidly repaired, DPCs create obstacles that disturb DNA replication, transcription and DNA damage repair, ultimately leading to genome instability. The persistence of DPCs

Repair of topoisomerase 1-induced DNA damage by tyrosyl-DNA phosphodiesterase 2 (TDP2) is dependent on its magnesium binding.

Naoto Shimizu et al.

The Journal of biological chemistry, 299(8), 104988-104988 (2023-07-02)

Topoisomerases are enzymes that relax DNA supercoiling during replication and transcription. Camptothecin, a topoisomerase 1 (TOP1) inhibitor, and its analogs trap TOP1 at the 3'-end of DNA as a DNA-bound intermediate, resulting in DNA damage that can kill cells. Drugs

TDP1-independent pathways in the process and repair of TOP1-induced DNA damage.

Huimin Zhang et al.

Nature communications, 13(1), 4240-4240 (2022-07-23)

Anticancer drugs, such as camptothecin (CPT), trap topoisomerase I (TOP1) on DNA and form TOP1 cleavage complexes (TOP1cc). Alternative repair pathways have been suggested in the repair of TOP1cc. However, how these pathways work with TDP1, a key repair enzyme

The protease SPRTN and SUMOylation coordinate DNA-protein crosslink repair to prevent genome instability.

Annamaria Ruggiano et al.

Cell reports, 37(10), 110080-110080 (2021-12-09)

DNA-protein crosslinks (DPCs) are a specific type of DNA lesion in which proteins are covalently attached to DNA. Unrepaired DPCs lead to genomic instability, cancer, neurodegeneration, and accelerated aging. DPC proteolysis was recently identified as a specialized pathway for DPC

Lipid-derived electrophiles mediate the effects of chemotherapeutic topoisomerase I poisons.

Amy Flor et al.

Cell chemical biology, 28(6), 776-787 (2020-12-23)

Topoisomerase 1 (Top1) reversibly nicks chromosomal DNA to relax strain accumulated during transcription, replication, chromatin assembly, and chromosome condensation. The Top1 poison camptothecin targets cancer cells by trapping the enzyme in the covalent complex Top1cc, tethered to cleaved DNA by

Topoisomerase 1 cleavage complex enables pattern recognition and inflammation during senescence.

Bo Zhao et al.

Nature communications, 11(1), 908-908 (2020-02-23)

Cyclic cGMP-AMP synthase (cGAS) is a pattern recognition cytosolic DNA sensor that is essential for cellular senescence. cGAS promotes inflammatory senescence-associated secretory phenotype (SASP) through recognizing cytoplasmic chromatin during senescence. cGAS-mediated inflammation is essential for the antitumor effects of immune

The chromatin structuring protein HMGA2 influences human subtelomere stability and cancer chemosensitivity.

Syed Moiz Ahmed et al.

PloS one, 14(5), e0215696-e0215696 (2019-05-09)

The transient build-up of DNA supercoiling during the translocation of replication forks threatens genome stability and is controlled by DNA topoisomerases (TOPs). This crucial process has been exploited with TOP poisons for cancer chemotherapy. However, pinpointing cellular determinants of the

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TDP1 suppresses chromosomal translocations and cell death induced by abortive TOP1 activity during gene transcription.

Diana Rubio-Contreras et al.

Nature communications, 14(1), 6940-6940 (2023-11-10)

DNA topoisomerase I (TOP1) removes torsional stress by transiently cutting one DNA strand. Such cuts are rejoined by TOP1 but can occasionally become abortive generating permanent protein-linked single strand breaks (SSBs). The repair of these breaks is initiated by tyrosyl-DNA

PARP-1-dependent RND1 transcription induced by topoisomerase I cleavage complexes confers cellular resistance to camptothecin.

Laetitia Mouly et al.

Cell death & disease, 9(9), 931-931 (2018-09-14)

RHO GTPases regulate essential functions such as the organization of the actin cytoskeleton. The classic members cycle between an active GTP-bound and an inactive GDP-bound conformation whereas atypical members are predominantly GTP-bound. Besides their well-established role, the classic RHO GTPases

Mitochondrial protein-linked DNA breaks perturb mitochondrial gene transcription and trigger free radical-induced DNA damage.

Shih-Chieh Chiang et al.

Science advances, 3(4), e1602506-e1602506 (2017-05-17)

Breakage of one strand of DNA is the most common form of DNA damage. Most damaged DNA termini require end-processing in preparation for ligation. The importance of this step is highlighted by the association of defects in the 3'-end processing

Topoisomerase 1 Regulates Gene Expression in Neurons through Cleavage Complex-Dependent and -Independent Mechanisms.

Angela M Mabb et al.

PloS one, 11(5), e0156439-e0156439 (2016-05-28)

Topoisomerase 1 (TOP1) inhibitors, including camptothecin and topotecan, covalently trap TOP1 on DNA, creating cleavage complexes (cc's) that must be resolved before gene transcription and DNA replication can proceed. We previously found that topotecan reduces the expression of long (>100

Defective repair of topoisomerase I induced chromosomal damage in Huntington's disease.

Nelma M Palminha et al.

Cellular and molecular life sciences : CMLS, 79(3), 160-160 (2022-03-01)

Topoisomerase1 (TOP1)-mediated chromosomal breaks are endogenous sources of DNA damage that affect neuronal genome stability. Whether TOP1 DNA breaks are sources of genomic instability in Huntington's disease (HD) is unknown. Here, we report defective 53BP1 recruitment in multiple HD cell

Tdp1 protects from topoisomerase 1-mediated chromosomal breaks in adult zebrafish but is dispensable during larval development.

Ringaile Zaksauskaite et al.

Science advances, 7(5) (2021-01-31)

Deficiency in the DNA end-processing enzyme, tyrosyl-DNA phosphodiesterase 1 (TDP1), causes progressive neurodegeneration in humans. Here, we generated a tdp1 knockout zebrafish and confirmed the lack of TDP1 activity. In adulthood, homozygotes exhibit hypersensitivity to topoisomerase 1 (Top1) poisons and

Targeting neddylation sensitizes colorectal cancer to topoisomerase I inhibitors by inactivating the DCAF13-CRL4 ubiquitin ligase complex.

Yilun Sun et al.

Nature communications, 14(1), 3762-3762 (2023-06-24)

Colorectal cancers (CRCs) are prevalent worldwide, yet current treatments remain inadequate. Using chemical genetic screens, we identify that co-inhibition of topoisomerase I (TOP1) and NEDD8 is synergistically cytotoxic in human CRC cells. Combination of the TOP1 inhibitor irinotecan or its

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