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Human Monoclonal TPI1 Primary Antibody for ELISA, WB - ABIN563235
Lee, Jiang, Sit, Wan: Proteome of human T lymphocytes with treatment of cyclosporine and polysaccharopeptide: analysis of significant proteins that manipulate T cells proliferation and immunosuppression. in International immunopharmacology 2007
Show all 3 Pubmed References
Human Monoclonal TPI1 Primary Antibody for ELISA, WB - ABIN521061
Smith, Qutob, Watson, Beavis, Potts, Welham, Garimella, Lind, Drew, Cawkwell: Proteomic identification of putative biomarkers of radiotherapy resistance: a possible role for the 26S proteasome? in Neoplasia (New York, N.Y.) 2009
Cow (Bovine) Polyclonal TPI1 Primary Antibody for WB - ABIN2783242
Ralser, Nebel, Kleindorp, Krobitsch, Lehrach, Schreiber, Reinhardt, Timmermann: Sequencing and genotypic analysis of the triosephosphate isomerase (TPI1) locus in a large sample of long-lived Germans. in BMC genetics 2008
A guide to the effects of a large portion of the residues of triosephosphate isomerase on catalysis, stability, druggability, and human disease has been presented. (Review)
Results revealed that TPI expression might be considered as a novel prognostic factor to evaluate gastric cancer patients' survival
TPI1 functions as a tumor suppressor in hepatocellular carcinoma and might serve as a potential therapeutic target for the treatment of HCC (show FAM126A Antibodies)
our findings are the first to identify, to our knowledge, a functional synaptic defect in TPI deficiency derived from molecular changes in the TPI dimer interface.
Polyvinylpyrrolidone stabilised silver nanoparticles (60 nM; 2-6 nm diameter) selectively inhibited PfTIM with a 7-fold decrease in enzyme catalytic efficiency (K(cat)/K (show CTSK Antibodies)(m)) over hTIM (show TIMELESS Antibodies).
results suggest amyloid-beta oligomers induce neuronal death by triggering methylglyoxal(MG) production; increased release of MG is a direct consequence of triosephosphate isomerase nitrotyrosination due to amyloid-beta peptide action at the 2 tyrosines associated with the catalytic center
TPI-PEP (show PAEP Antibodies) co-crystal structure, demonstrating that PEP (show PAEP Antibodies) directly binds into the catalytic pocket of TPI.
Data suggest that exchange reactions during gluconeogenesis catalyzed by triose-phosphate isomerase and transaldolase (show TALDO1 Antibodies) do not differ between subjects with type 2 diabetes and control subjects under fasting or hyperglycemic conditions.
we review the relationship between modified TPI and Alzheimer disease (AD), highlighting the relevance of this protein in AD pathology
study found promoter SNPs of CKB (show CHKB Antibodies) and TPI1 were weakly associated with schizophrenia;in addition, IFNG (show IFNG Antibodies) polymorphisms were associated with schizophrenia; results suggest that IFNG (show IFNG Antibodies) and proteins affected by IFNG (show IFNG Antibodies) may play a role in the pathogenesis of schizophrenia
TPI interacts with Tau protein in a normal, nondisease state as well as in a neurodegenerative state.
Triosephosphate isomerase activity-deficient mice show haemolytic anaemia in homozygous condition
data indicate that Tipin (show TIPIN Antibodies)/Tim1 (show TIMELESS Antibodies)/And1 (show WDHD1 Antibodies) form a complex that links stabilization of replication fork and establishment of sister chromatid cohesion
Sperm TPI content and amounts of GPX5 in seminal plasma may be used as quality markers of boar sperm.
TPI sugarkill can be genetically complemented by TPI encoding a catalytically inactive enzyme.
Mutation of wasted away, a recessive, hypomorphic mutation of triosephosphate isomerase (Tpi), highlights the essential protective role of triosephosphate isomerase.
This gene encodes an enzyme, consisting of two identical proteins, which catalyzes the isomerization of glyceraldehydes 3-phosphate (G3P) and dihydroxy-acetone phosphate (DHAP) in glycolysis and gluconeogenesis. Mutations in this gene are associated with triosephosphate isomerase deficiency. Pseudogenes have been identified on chromosomes 1, 4, 6 and 7. Alternative splicing results in multiple transcript variants.
, triosephosphate isomerase
, triosephosphate isomerase 1
, Triose-phosphate isomerase
, triosephosphate isomerase (TIM, D-glyceraldehyde 3-phosphate ketol-isomerase)
, triosephoshpate isomerase
, neurodegeneration 14
, triose phosphate isomerase
, wasted away