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SLC25A19 encodes a mitochondrial protein that is a member of the solute carrier family. Additionally we are shipping Solute Carrier Family 25 (Mitochondrial Thiamine Pyrophosphate Carrier), Member 19 Antibodies (30) and many more products for this protein.
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Chronic alcohol exposure negatively impacts pancreatic mitochondrial thiamin pyrophosphate transport, and this effect is exerted, at least in part, at the level of Slc25a19 transcription and appears to involve an epigenetic mechanism.
mitochondria of Slc25a19(-/-) and Amish lethal microcephaly cells have undetectable and markedly reduced thiamine pyrophosphate content, respectively
We review the evidence that the function of the SLC25A19 gene product, previously identified as the mitochondrial deoxyribonucleotide carrier (DNC), is actually the transport of thiamine pyrophosphate.[review]
Pancreatic acinar cells Mitochondrial Thiamin Pyrophosphate uptake process is adaptively regulated by the prevailing thiamin level and this regulation is exerted at the level of transcription of the SLC25A19 gene and involves transcription factor binding affinity/epigenetic mechanisms.
Among 6 residues predicted by the docking model ( Thr (show TRH Proteins)(29), Arg(30), Ile(33), Ser (show SIGLEC1 Proteins)(34), Asp (show ASIP Proteins)(37) and Phe(298)), only Ile(33), Ser (show SIGLEC1 Proteins)(34) and Asp (show ASIP Proteins)(37) were critical for function. Ser (show SIGLEC1 Proteins)(34) did not affect translation/stability. Ile(33) and Asp (show ASIP Proteins)(37) mutants decreased this parameter andwere expressed less in mitochondria. A polar residue was needed at position 34. His(137) and Lys (show LYZ Proteins)(291) are needed for delivery to mitochondria.
These findings demonstrate that the genes involved in dictating thiamine homeostasis, such as SLC19A2, SLC25A19 and TPK-1, were significantly up-regulated in clinical tissues and breast cancer cell lines.
Characterization of the SLC25A19 promoter and demonstration of an essential role for NF-Y in its basal activity.
Compares and contrasts all the known human SLC25A (show SLC25A25 Proteins)* genes and includes functional information.
mutant protein lacks the normal transport activity, implying that failed deoxynucleotide transport across the inner mitochondrial membrane causes Amiah microcephaly (MCPHA)
a pathogenic missense mutation in the SLC25A19 gene was identifiedin 4 patients who suffered from recurrent episodes of flaccid paralysis and encephalopathy associated with bilateral striatal necrosis and chronic progressive polyneuropathy
This gene encodes a mitochondrial protein that is a member of the solute carrier family. Although this protein was initially thought to be the mitochondrial deoxynucleotide carrier involved in the uptake of deoxynucleotides into the matrix of the mitochondria, further studies have demonstrated that this protein instead functions as the mitochondrial thiamine pyrophosphate carrier, which transports thiamine pyrophosphates into mitochondria. Mutations in this gene cause microcephaly, Amish type, a metabolic disease that results in severe congenital microcephaly, severe 2-ketoglutaric aciduria, and death within the first year. Multiple alternatively spliced variants, encoding the same protein, have been identified for this gene.
mitochondrial thiamine pyrophosphate carrier
, solute carrier family 25, member 19
, solute carrier family 25 (mitochondrial deoxynucleotide carrier), member 19
, solute carrier family 25 member 19
, solute carrier family 25 (mitochondrial thiamine pyrophosphate carrier), member 19
, microcephaly, Amish
, mitochondrial uncoupling protein 1
, mitochondrial deoxynucleotide carrier
, Mitochondrial deoxynucleotide carrier