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SLC25A46 belongs to the SLC25 family of mitochondrial carrier proteins (Haitina et al., 2006 [PubMed 16949250]).[supplied by OMIM, Mar 2008].. Zusätzlich bieten wir Ihnen SLC25A46 Proteine (3) und und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal SLC25A46 Primary Antibody für WB - ABIN4244462
Duchesne, Vaiman, Castille, Beauvallet, Gaignard, Floriot, Rodriguez, Vilotte, Boulanger, Passet, Albaric, Guillaume, Boukadiri, Richard, Bertaud, Timsit, Guatteo, Jaffrézic, Calvel, Helary, Mahla et al.: Bovine and murine models highlight novel roles for SLC25A46 in mitochondrial dynamics and metabolism, with implications for human and animal health. ... in PLoS genetics 2017
recently, the "Turning calves syndrome", a novel sensorimotor polyneuropathy was described in the French Rouge-des-Pres cattle breed. In the present study, we determined that this hereditary disease resulted from a single nucleotide substitution in SLC25A46, a gene encoding a protein of the mitochondrial carrier family. This mutation caused an apparent damaging amino-acid substitution.
This study reported a novel variant (p.Trp160Ser) in SLC25A46 and we broaden the phenotypic spectrum associated with mutations in SLC25A46.
This study identified of a homozygous missense mutation c.1022T>C and a homozygous genomic deletion involving exon 1 in SLC25A46 encoding a mitochondrial protein (zeige COX6B2 Antikörper) leading to lethal pontocerebellar hypoplasia with apnoea and profound weakness.
These results show that SLC25A46 plays a role in a mitochondrial/endoplasmic reticulum pathway that facilitates lipid transfer, and link altered mitochondrial dynamics to early-onset neurodegenerative disease and cell fate decisions.
SLC25A46 is selectively degraded from the outer membrane independently of mitophagy and apoptosis, providing a framework for mechanistic studies in the proteolysis of outer membrane proteins
we showed that the Slc25a46 disruption caused a fusion/fission imbalance and an abnormal mitochondrial architecture that disturbed mitochondrial metabolism. These data extended the range of phenotypes associated with Slc25a46 dysfunction. Moreover, this Slc25a46 knock-out mouse model should be useful to further elucidate the role of SLC25A46 in mitochondrial dynamics
Our mutant mice provide a valid model for understanding the mechanistic basis of the complex SLC25A46-mediated pathologies, as well as for screening potential therapeutic interventions.
Data indicate four families with recessive mutations in solute carrier family 25 member 46 protein (SLC25A46).
Compares and contrasts all the known human SLC25A (zeige SLC25A25 Antikörper)* genes and includes functional information.
SLC25A46 belongs to the SLC25 family of mitochondrial carrier proteins (Haitina et al., 2006
solute carrier family 25, member 46
, solute carrier family 25 member 46-like
, solute carrier family 25 member 46
, solute carrier family 25 member 46-B