Study of UV-induced DNA Repair Factor Recruitment: Kinetics and Dynamics

2017 ◽  
pp. 101-105 ◽  
Author(s):  
Sarah Sertic ◽  
Stefania Roma ◽  
Paolo Plevani ◽  
Federico Lazzaro ◽  
Marco Muzi-Falconi
Keyword(s):  
Dna Repair ◽  
Kinetics And Dynamics ◽  
Repair Factor

scholarly journals Two Sides of the Same Coin: TFIIH Complexes in Transcription and DNA Repair

2010 ◽  
Vol 10 ◽  
pp. 633-643 ◽  
Author(s):  
Alexander Zhovmer ◽  
Valentyn Oksenych ◽  
Frédéric Coin
Keyword(s):  
Dna Repair ◽  
Western Blotting ◽  
Chromatin Immunoprecipitation ◽  
Transcription Initiation ◽  
Dna Lesions ◽  
Dynamic Composition ◽  
The Core ◽  
Repair Factor ◽  
A New Technique ◽  
Two Sides

TFIIH is organized into a seven-subunit core associated with a three-subunit Cdk-activating kinase (CAK) module. TFIIH has roles in both transcription initiation and DNA repair. During the last 15 years, several studies have been conducted to identify the composition of the TFIIH complex involved in DNA repair. Recently, a new technique combining chromatin immunoprecipitation and western blotting resolved the hidden nature of the TFIIH complex participating in DNA repair. Following the recruitment of TFIIH to the damaged site, the CAK module is released from the core TFIIH, and the core subsequently associates with DNA repair factors. The release of the CAK is specifically driven by the recruitment of the DNA repair factor XPA and is required to promote the incision/excision of the damaged DNA. Once the DNA lesions have been repaired, the CAK module returns to the core TFIIH on the chromatin, together with the release of the repair factors. These data highlight the dynamic composition of a fundamental cellular factor that adapts its subunit composition to the cell needs.

scholarly journals Erratum: Ubiquitous overexpression of the DNA repair factor dPrp19 reduces DNA damage and extends Drosophila life span

2017 ◽  
Vol 3 (1) ◽  
Author(s):  
Kathrin Garschall ◽  
Hanna Dellago ◽  
Martina Gáliková ◽  
Markus Schosserer ◽  
Thomas Flatt ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Life Span ◽  
Repair Factor

The V(D)J Recombination/DNA Repair Factor Artemis Belongs to the Metallo-β-Lactamase Family and Constitutes a Critical Developmental Checkpoint of the Lymphoid System

2003 ◽  
Vol 987 (1) ◽  
pp. 150-157 ◽  
Author(s):  
DESPINA MOSHOUS ◽  
ISABELLE CALLEBAUT ◽  
RÉGINA CHASSEVAL ◽  
CATHERINE POINSIGNON ◽  
ISABELLE VILLEY ◽  
...  
Keyword(s):  
Dna Repair ◽  
Lymphoid System ◽  
Repair Factor

Impaired Expression of the DNA Repair Factor DDB2 in Human Myeloid Leukemias.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2046-2046
Author(s):  
Rishu Takimoto ◽  
Junji Kato ◽  
Koichi Takada ◽  
Takuya Matsunaga ◽  
Yoshiro Niitsu
Keyword(s):  
Dna Repair ◽  
Excision Repair ◽  
Leukemia Cell ◽  
K562 Cells ◽  
Leukemic Cells ◽  
Repair System ◽  
Myeloid Leukemias ◽  
Repair Factor ◽  
Human Leukemic Cells ◽  
Damaged Dna

Abstract Recent studies have suggested that chromosomal deletions might represent a mechanism of inactivation of DNA repair system in various hematological malignancies, including myeloid leukemias. However, the precise mechanisms remain unclear. Damaged DNA binding protein-2 (DDB2), a DNA repair factor induced by tumor suppressor p53, plays an important role in the nucleotide excision repair of UV-damaged DNA. Despite frequent mutations of p53 in human leukemic cells, the role of DDB2 on the leukemogenesis is unkown. In this study, we examined expression of DDB2 mRNA in four human myeloid leukemia cell lines (K562, KG1, HL60, and MEG01) and in fresh leukemic cells obtained from 4 patients with myeloid leukemias. In all leukemia cells, expression of DDB2 mRNA was remarkably decreased as compared to that of CD34 cells We then assayed DDB2-dependent DNA repairing activity in the leukemic cells using specific antibodies against photoproducts, and found that DNA repairing activity was reduced. When a plasmid encoding DDB2 gene (pCV-DDB2) was transduced into K562 cells, the DNA repairing activity was significantly restored. Finally we tested the expression of DDB2 mRNA in five myeloid leukemias obtained from patients, and found loss of DDB2 expression in four patients. These results suggested that in human myeloid leukemias, suppression of DDB2 expression may contribute to accumulation of gene mutation through the dysfunction of DNA repair.

PARP-1 regulation of DNA repair factor availability.

2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 269-269
Author(s):  
Matthew Joseph Schiewer ◽  
Amy C Mandigo ◽  
Nicolas Gordon ◽  
Christopher McNair ◽  
Costas D. Lallas ◽  
...  
Keyword(s):  
Dna Repair ◽  
Transcriptional Profiling ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Damage Repair ◽  
Mechanistic Investigation ◽  
Androgen Receptor Activity ◽  
Repair Factor ◽  
Parp 1

269 Background: PARP-1 holds major functions on chromatin, DNA damage repair and transcriptional regulation, both of which are relevant in the context of cancer. Previously, it was determined that PARP-1 ins involved in regulation of androgen receptor activity. Methods: Here, unbiased transcriptional profiling revealed the downstream transcriptional profile of PARP-1 enzymatic activity.Results: Further investigation of the PARP-1-regulated transcriptome and secondary strategies for assessing PARP-1 activity in patient tissues revealed that PARP-1 activity was unexpectedly enriched as a function of disease progression and was associated with poor outcome independent of DNA double-strand breaks, suggesting that enhanced PARP-1 activity may promote aggressive phenotypes. Mechanistic investigation revealed that active PARP-1 served to enhance E2F1 transcription factor activity, and specifically promoted E2F1-mediated induction of DNA repair factors involved in homologous recombination (HR). Conversely, PARP-1 inhibition reduced HR factor availability and thus acted to induce or enhance “BRCA-ness”. Conclusions: These observations bring new understanding of PARP-1 function in cancer and have significant ramifications on predicting PARP-1 inhibitor function in the clinical setting.

scholarly journals DNA damage in 3D constricted migration or after lamin-A depletion in 2D: shared mechanisms of repair factor mis-localization under nuclear stress

2016 ◽  
Author(s):  
Yuntao Xia ◽  
Jerome Irianto ◽  
Charlotte R. Pfeifer ◽  
Jiazheng Ji ◽  
Irena L. Ivanovska ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Nuclear Envelope ◽  
Nuclear Structure ◽  
Lamin A ◽  
Soft Matrix ◽  
Progeroid Syndromes ◽  
Standard Culture ◽  
Repair Factor ◽  
Insight Into

AbstractCells that migrate through small, rigid pores and that have normal levels of the nuclear structure protein lamin-A exhibit an increase in DNA damage, which is also observed with lamin-A depletion in diseases such as cancer and with many lamin-A mutations. Here we show nuclear envelope rupture is a shared feature that increases in standard culture after lamin-A knockdown, which causes nuclear loss of multiple DNA repair factors and increased DNA damage. Some repair factors are merely mis-localized to cytoplasm whereas others are partially depleted unless rescued by lamin-A expression. Compared to standard cultures on rigid glass coverslips, the growth of lamin-A low cells on soft matrix relaxes cytoskeletal stress on the nucleus, suppresses the mis-localization of DNA repair factors, and minimizes DNA damage nearly to wildtype levels. Conversely, constricted migration of the lamin-A low cells causes abnormally high levels of DNA damage, consistent with sustained loss of repair factors. The findings add insight into why monogenic progeroid syndromes that often associate with increased DNA damage and predominantly impact cells in stiff tissues result from mutations only in lamin-A or DNA repair factors.

Abstract B017: PARP-1 and E2F1 collaborate to transcriptionally regulate DNA repair factor availability

2018 ◽  
Author(s):  
Matthew J. Schiewer ◽  
Amy Mandigo ◽  
Nicolas Gordon ◽  
Fangjin Huang ◽  
Sanchaika Gaur ◽  
...  
Keyword(s):  
Dna Repair ◽  
Repair Factor ◽  
Parp 1
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