Results 11 to 20 of about 2,696,015 (152)

Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes [PDF]

open access: yesEMBO Molecular Medicine, 2021
WW domain‐containing oxidoreductase (WWOX) is an emerging neural gene‐regulating homeostasis of the central nervous system. Germline biallelic mutations in WWOX cause WWOX‐related epileptic encephalopathy (WOREE) syndrome and spinocerebellar ataxia and ...
Srinivasarao Repudi   +4 more
doaj   +3 more sources

Molecular Biology of the WWOX Gene That Spans Chromosomal Fragile Site FRA16D [PDF]

open access: yesCells, 2021
It is now more than 20 years since the FRA16D common chromosomal fragile site was characterised and the WWOX gene spanning this site was identified. In this time, much information has been discovered about its contribution to disease; however, the normal
Cheng Shoou Lee   +4 more
doaj   +4 more sources

Novel homozygous mutation in the WWOX gene causes seizures and global developmental delay: Report and review [PDF]

open access: yesTranslational Neuroscience, 2018
The WWOX gene has a WW domain containing oxidoreductase, which is located at the common fragile site FRA16D at chromosome 16q23. WWOX is a tumor suppressor gene that has been associated with several types of cancer such as hepatic, breast, lung, prostate,
Ehaideb Salleh N.   +4 more
doaj   +3 more sources

Epigenetic and genetic alterations affect the WWOX gene in head and neck squamous cell carcinoma. [PDF]

open access: yesPLoS ONE, 2015
Different types of genetic and epigenetic changes are associated with HNSCC. The molecular mechanisms of HNSCC carcinogenesis are still undergoing intensive investigation.
Seda Ekizoglu   +4 more
doaj   +3 more sources

Association of WWOX Gene Expression with Chronic Lymphocytic Leukemia [PDF]

open access: yesNamık Kemal Tıp Dergisi, 2020
Aim:The WW domain-containing oxidoreductase (WWOX) gene is located on chromosome 16q23.3-q24.1 and contains the common chromosomal fragile site, FRA16D. The WWOX gene encodes a Wwox tumor suppressor protein with a molecular weight of 46 kDa.
Halil HANCI   +4 more
doaj   +2 more sources

Identification of compound heterozygous deletion of the WWOX gene in WOREE syndrome [PDF]

open access: yesBMC Medical Genomics, 2023
Background Biallelic loss-of-function variants in WWOX cause WWOX-related epileptic encephalopathy (WOREE syndrome), which has been reported in 60 affected individuals to date.
Xing-sheng Dong   +5 more
doaj   +2 more sources

The WWOX Gene Influences Cellular Pathways in the Neuronal Differentiation of Human Neural Progenitor Cells [PDF]

open access: yesFrontiers in Cellular Neuroscience, 2019
The brain is the most functionally organized structure of all organs. It manages behavior, perception and higher cognitive functions. The WWOX gene is non-classical tumor suppressor gene, which has been shown to have an impact on proliferation, apoptosis
Katarzyna Kośla   +5 more
doaj   +2 more sources

WWOX Modulates ROS-Dependent Senescence in Bladder Cancer

open access: yesMolecules, 2022
The tumor-suppressor gene, WW domain-containing oxidoreductase (WWOX), has been found to be lost in various types of cancers. ROS result as a tightly regulated signaling process for the induction of cell senescence.
Ching-Wen Liu   +4 more
doaj   +2 more sources

Functional genetic variant of WW domain-containing oxidoreductase (WWOX) gene is associated with hepatocellular carcinoma risk. [PDF]

open access: yesPLoS ONE, 2017
BACKGROUND:Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide. Human WW domain-containing oxidoreductase (WWOX) gene has been identified as a tumor suppressor gene in multiple cancers.
Hsiang-Lin Lee   +5 more
doaj   +2 more sources

Generation and characterization of mice carrying a conditional allele of the Wwox tumor suppressor gene.

open access: yesPLoS ONE, 2009
WWOX, the gene that spans the second most common human chromosomal fragile site, FRA16D, is inactivated in multiple human cancers and behaves as a suppressor of tumor growth.
John H Ludes-Meyers   +5 more
doaj   +2 more sources

Home - About - Disclaimer - Privacy