Results 11 to 20 of about 7,414 (159)

Fanconi anemia proteins function in mitophagy and immunity [PDF]

Cell, 2016
Fanconi anemia (FA) pathway genes are important tumor suppressors whose best-characterized function is repair of damaged nuclear DNA. Here, we describe an essential role for FA genes in two forms of selective autophagy.
Clapp, D. Wade, Dong, Xiaonan, Fernández, Álvaro F., Franco, Luis, Hanenberg, Helmut, Lee, Ming Yeh, Levine, Beth, Marchal, Christophe, Sirasanagandla, Shyam, Sumpter Jr., Rhea, Wei, Yongjie, Zou, Zhongju   +11 more
core   +3 more sources

Betulinic Acid Suppresses UBE2T Expression via MAPK/ERK Inhibition to Block FANCI and FANCD2 Monoubiquitination in Glioblastoma. [PDF]

J Cell Mol Med
ABSTRACT Platinum‐based chemotherapy remains a cornerstone of glioma treatment, yet resistance driven by the Fanconi anaemia (FA) DNA repair pathway limits efficacy. Here, we identified betulinic acid (BA) as a potent inhibitor of FA pathway activation.
Bao Y, Wang M.
europepmc   +2 more sources

Fanconi Anemia complementation group C protein in metabolic disorders

Aging, 2018
Given importance of 22-Fanconi Anemia (FA) proteins together to act in a signaling pathway in preventing deleterious clinical symptoms, e.g. severe bone marrow failure, congenital defects, an early onset of aging and cancer, studies on each FA protein become increasingly attractive.
Nepal, Manoj, Ma, Chi, Xie, Guoxiang, Jia, Wei, Fei, Peiwen   +4 more
openaire   +2 more sources

Fanconi anemia (FA) binding protein FAAP20 stabilizes FA complementation group A (FANCA) and participates in interstrand cross-link repair [PDF]

Proceedings of the National Academy of Sciences, 2012
The Fanconi anemia (FA) pathway participates in interstrand cross-link (ICL) repair and the maintenance of genomic stability. The FA core complex consists of eight FA proteins and two Fanconi anemia-associated proteins (FAAP24 and FAAP100). The FA core complex has ubiquitin ligase activity responsible for monoubiquitination of the FANCI-FANCD2 (ID ...
Chen, J, Leung, JWC, Wang, Y, Fong, KW, Huen, MSY, Li, L   +5 more
openaire   +4 more sources

Phosphorylation of Fanconi Anemia (FA) Complementation Group G Protein, FANCG, at Serine 7 Is Important for Function of the FA Pathway [PDF]

Journal of Biological Chemistry, 2004
Fanconi anemia (FA) is an autosomal recessive disease of cancer susceptibility. FA cells exhibit a characteristic hypersensitivity to DNA cross-linking agents. The molecular mechanism for the disease is unknown as few of the FA proteins have functional motifs. Several post-translational modifications of the proteins have been described.
Fengyu, Qiao, Jun, Mi, James B, Wilson, Gang, Zhi, Natalie R, Bucheimer, Nigel J, Jones, Gary M, Kupfer   +6 more
openaire   +2 more sources

A deficiency in a 230 kDa DNA repair protein in Fanconi anemia complementation group A cells is corrected by the FANCA cDNA [PDF]

Carcinogenesis, 1999
Cells from individuals with the cancer-prone, inherited disorder Fanconi anemia (FA) are hypersensitive to DNA interstrand cross-linking agents and this hypersensitivity correlates with a defect in ability to repair this type of damage to their DNA. We have isolated a DNA endonuclease complex from the nuclei of normal human cells which is involved in ...
D W, Brois, L W, McMahon, N I, Ramos, L M, Anglin, C E, Walsh, M W, Lambert   +5 more
openaire   +2 more sources

Identification of the Fanconi Anemia Complementation Group I Gene, FANCI

Cellular Oncology, 2007
To identify the gene underlying Fanconi anemia (FA) complementation group I we studied informative FA-I families by a genome-wide linkage analysis, which resulted in 4 candidate regions together encompassing 351 genes.
Josephine C. Dorsman, Marieke Levitus, Davy Rockx, Martin A. Rooimans, Anneke B. Oostra, Anneke Haitjema, Sietske T. Bakker, Jûrgen Steltenpool, Dezsö Schuler, Sheila Mohan, Detlev Schindler, Fré Arwert, Gerard Pals, Christopher G. Mathew, Quinten Waisfisz, Johan P. de Winter, Hans Joenje   +16 more
doaj   +1 more source

Preclinical correction of human Fanconi anemia complementation group A bone marrow cells using a safety-modified lentiviral vector. [PDF]

, 2010
One of the major hurdles for the development of gene therapy for Fanconi anemia (FA) is the increased sensitivity of FA stem cells to free radical-induced DNA damage during ex vivo culture and manipulation.
Adair, J, Beard, BC, Becker, PS, Chien, S, Kiem, H-P, Kohn, DB, Shimamura, A, Taylor, JA, Trobridge, GD, Wagner, JE, Zhao, X   +10 more
core   +2 more sources

An Arabidopsis FANCJ helicase homologue is required for DNA crosslink repair and rDNA repeat stability.

PLoS Genetics, 2019
Proteins of the Fanconi Anemia (FA) complementation group are required for crosslink (CL) repair in humans and their loss leads to severe pathological phenotypes.
Annika Dorn, Laura Feller, Dominique Castri, Sarah Röhrig, Janina Enderle, Natalie J Herrmann, Astrid Block-Schmidt, Oliver Trapp, Laura Köhler, Holger Puchta   +9 more
doaj   +1 more source

Bioinformatics and Experimental Evaluation of UBE2W and SSX2IP Expression Levels in HepG2 Cancer Cells Treated with Melatonin

Journal of Mazandaran University of Medical Sciences, 2021
Background and purpose: The aim of this study was to bioinformatically and experimentally evaluate the effect of melatonin on the expression levels of UBE2W and SSX2IP genes in melatonin treated Human Hepatocellular carcinoma G2 (HepG2) cancer cell line.
Ali Rajabi, Ali Emami, Behnaz Barzegarzadeh Namarvar, Reza Safaralizadeh   +3 more
doaj