Ask about this productRelated genes to: VARS Blocking Peptide
- Gene:
- VARS NIH gene
- Name:
- valyl-tRNA synthetase
- Previous symbol:
- VARS2
- Synonyms:
- -
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-18
- Date modifiied:
- 2016-10-05
- Gene:
- VARS2 NIH gene
- Name:
- valyl-tRNA synthetase 2, mitochondrial
- Previous symbol:
- VARS2L, VARSL
- Synonyms:
- DKFZP434L1435, KIAA1885, G7a
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-02
- Date modifiied:
- 2014-11-19
Related products to: VARS Blocking Peptide
Related articles to: VARS Blocking Peptide
- Transfer RNA dynamics contribute to cancer development through regulation of codon-specific messenger RNA translation. Specific aminoacyl-tRNA synthetases can either promote or suppress tumourigenesis. Here we show that valine aminoacyl-tRNA synthetase (VARS) is a key player in the codon-biased translation reprogramming induced by resistance to targeted (MAPK) therapy in melanoma. The proteome rewiring in patient-derived MAPK therapy-resistant melanoma is biased towards the usage of valine and coincides with the upregulation of valine cognate tRNAs and of VARS expression and activity. Strikingly, VARS knockdown re-sensitizes MAPK-therapy-resistant patient-derived melanoma in vitro and in vivo. Mechanistically, VARS regulates the messenger RNA translation of valine-enriched transcripts, among which hydroxyacyl-CoA dehydrogenase mRNA encodes for a key enzyme in fatty acid oxidation. Resistant melanoma cultures rely on fatty acid oxidation and hydroxyacyl-CoA dehydrogenase for their survival upon MAPK treatment. Together, our data demonstrate that VARS may represent an attractive therapeutic target for the treatment of therapy-resistant melanoma. - Source: PubMed
Publication date: 2024/06/07
El-Hachem NajlaLeclercq MarineSusaeta Ruiz MiguelVanleyssem RaphaelShostak KaterynaKörner Pierre-RenéCapron CoralieMartin-Morales LorenaRoncarati PatrickLavergne ArnaudBlomme ArnaudTurchetto SilviaGoffin EricThandapani PalanirajaTarassov IvanNguyen LaurentPirotte BernardChariot AlainMarine Jean-ChristopheHerfs MichaelRapino FrancescaAgami ReuvenClose Pierre - After publication of the article [1], it has been brought to our attention that there is a nomenclature issue with this article. At the time of acceptance, the VARS2 mutation was considered equivalent to the VARS2 mutation. However, this has changed so that VARS now only refers to shorter mitochondrial sequence of valyl-tRNA synthesase containing 1093 amino acids. "Therefore, in the context of this article, every usage of "VARS2" should be replaced with "VARS" when referring to the causative variant". - Source: PubMed
Publication date: 2017/12/08
Alsemari AbdulazizAl-Younes BananGoljan EwaJaroudi DyalaBinHumaid FaisalMeyer Brian FArold Stefan TMonies Dorota - Germline stem cell proliferation is necessary to populate the germline with sufficient numbers of cells for gametogenesis and for signaling the soma to control organismal properties such as aging. The Caenorhabditis elegans gene glp-4 was identified by the temperature-sensitive allele bn2 where mutants raised at the restrictive temperature produce adults that are essentially germ cell deficient, containing only a small number of stem cells arrested in the mitotic cycle but otherwise have a morphologically normal soma. We determined that glp-4 encodes a valyl aminoacyl transfer RNA synthetase (VARS-2) and that the probable null phenotype is early larval lethality. Phenotypic analysis indicates glp-4(bn2ts) is partial loss of function in the soma. Structural modeling suggests that bn2 Gly296Asp results in partial loss of function by a novel mechanism: aspartate 296 in the editing pocket induces inappropriate deacylation of correctly charged Val-tRNA(val). Intragenic suppressor mutations are predicted to displace aspartate 296 so that it is less able to catalyze inappropriate deacylation. Thus glp-4(bn2ts) likely causes reduced protein translation due to decreased levels of Val-tRNA(val). The germline, as a reproductive preservation mechanism during unfavorable conditions, signals the soma for organismal aging, stress and pathogen resistance. glp-4(bn2ts) mutants are widely used to generate germline deficient mutants for organismal studies, under the assumption that the soma is unaffected. As reduced translation has also been demonstrated to alter organismal properties, it is unclear whether changes in aging, stress resistance, etc. observed in glp-4(bn2ts) mutants are the result of germline deficiency or reduced translation. - Source: PubMed
Publication date: 2015/10/13
Rastogi SuchitaBorgo BenPazdernik NanetteFox PaulMardis Elaine RKohara YujiHavranek JimSchedl Tim