Stitching up broken DNA ends by FANCA

Palovcak, Anna; Liu, Wenjun; Yuan, Fenghua; Zhang, Yanbin

doi:10.1080/23723556.2018.1518101

Cited by 3 publications

(3 citation statements)

References 10 publications

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“…It has been widely explored in therapeutics . To evaluate the siRNA transfection efficiency of the synthesized APCDs and APCDs-OA conjugates, two siRNA for silencing FANCA and FANCD2 proteins involved in DNA repair were selected as siRNA models. , The expression levels of FANCA and FANCD2 proteins in U2OS cells were analyzed by Western blot. Regarding vehicles, the mass ratio of the as-prepared material to siRNA was 40:1.…”

Section: Resultsmentioning

confidence: 99%

Gene Transfection Efficiency Improvement with Lipid Conjugated Cationic Carbon Dots

Chen,

Li,

Zhao

et al. 2024

ACS Appl. Mater. Interfaces

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Section: Resultsmentioning

confidence: 99%

Gene Transfection Efficiency Improvement with Lipid Conjugated Cationic Carbon Dots

Chen,

Li,

Zhao

et al. 2024

ACS Appl. Mater. Interfaces

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“…Palovcak A discovered that in a reconstitution system with purified proteins and various DNA substrates, FANCA, a protein central to FA pathway activation and function, catalyzes Single-Strand Annealing(SSA) and strand exchange of complementary DNA oligonucleotides. This property enables FANCA to directly participate in the SSA pathway of DSB repair in cells [ 31 ]. In our study, more FANCA mutations were found in PTMC patients, which may be related to the genomic instability caused by FANCA mutation and the decrease in DSB repair capacity.…”

Section: Discussionmentioning

confidence: 99%

DNA double-strand break repair gene mutation and the risk of papillary thyroid microcarcinoma: a case–control study

Qin

Fan

et al. 2021

Cancer Cell Int

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Objective To study the relationship between DNA double-strand break (DSB) repair gene mutations and the risk of papillary thyroid microcarcinoma (PTMC). Methods One hundred patients with PTMC or benign thyroid nodules (BTNs) at Henan Cancer Hospital were retrospectively analyzed. The DSB repair capacity of peripheral blood T lymphocytes in the two groups was assessed by flow cytometry. Data were compared using Student’s t-test to evaluate the relationship between DSB repair capacity and the risk of PTMC. Factors influencing DSB repair capacity were analyzed by multivariate logistic regression analysis. The relationship between PTMC and DSB repair capacity was analyzed by univariate analysis. Targeted next-generation DNA sequencing was applied to screen and analyze DSB repair genes related to PTMC. Results The DSB repair capacity was 31.30% in the PTMC group and 44.40% in the BTN group, with that of the former being significantly lower (P < 0.05). Multivariate logistic regression analysis of age, sex, obesity status, radiation and other factors showed that radiation exposure was positively correlated with reduced DSB repair capacity(OR = 3.642; 95% CI 1.484–8.935, P = 0.020). Moreover, univariate analysis showed that a reduction in DSB repair capacity was a risk factor for PTMC(OR = 2.333; 95% CI 1.027–5.300, P = 0.043).Targeted next-generation DNA sequencing was performed on the DSB repair genes discovered, and those that were mutated in association with PTMC were Rad50 and FANCA; Rad51 mutations were related to BTN. Conclusion Radiation exposure is positively associated with induced DSB repair gene mutations, which may cause a reduced capacity for DSB repair and eventually lead to PTMC.

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“…Accordingly, ICL sensitivity can be rescued by inhibition of many NHEJ factors in many FA deficiency models including C. elegans, chicken DT40 cells, mouse embryonic fibroblasts and human cells where FA components were knocked down, knocked out, or mutated [79,80]. Besides these two subpathways, SSA may also participate in ICL and DSB repair via the newly identified strand annealing activity of FANCA [66,81,82].…”

Section: Dsb Repair Through Hr and Other Sub-pathwaysmentioning

confidence: 99%

Fanconi anemia pathway as a prospective target for cancer intervention

Liu

Palovcak

et al. 2020

Cell Biosci

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Fanconi anemia (FA) is a recessive genetic disorder caused by biallelic mutations in at least one of 22 FA genes. Beyond its pathological presentation of bone marrow failure and congenital abnormalities, FA is associated with chromosomal abnormality and genomic instability, and thus represents a genetic vulnerability for cancer predisposition. The cancer relevance of the FA pathway is further established with the pervasive occurrence of FA gene alterations in somatic cancers and observations of FA pathway activation-associated chemotherapy resistance. In this article we describe the role of the FA pathway in canonical interstrand crosslink (ICL) repair and possible contributions of FA gene alterations to cancer development. We also discuss the perspectives and potential of targeting the FA pathway for cancer intervention.

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Stitching up broken DNA ends by FANCA

Cited by 3 publications

References 10 publications

Gene Transfection Efficiency Improvement with Lipid Conjugated Cationic Carbon Dots

Gene Transfection Efficiency Improvement with Lipid Conjugated Cationic Carbon Dots

DNA double-strand break repair gene mutation and the risk of papillary thyroid microcarcinoma: a case–control study

Fanconi anemia pathway as a prospective target for cancer intervention

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