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Tufm encodes a protein which participates in protein translation in mitochondria. Additionally we are shipping Tu Translation Elongation Factor, Mitochondrial Antibodies (70) and Tu Translation Elongation Factor, Mitochondrial Proteins (11) and many more products for this protein.
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study revealed a novel role for TUFM as a host restriction factor that exerts an inhibitory effect on avian-signature PB2627E influenza virus propagation in human cells; found that increased TUFM-dependent autophagy correlates with the inhibitory effect on avian-signature influenza virus replication and may serve as a key intrinsic mechanism to restrict avian influenza virus infection in humans
High expression of TUFM is associated with colorectal cancer.
we identify a novel signaling hub centering on the NLRX1 (show NLRX1 ELISA Kits) TUFM protein complex, promoting autophagic flux. Defects in the expression of either NLRX1 (show NLRX1 ELISA Kits) or TUFM result in compromised autophagy when treated with EGFR (show EGFR ELISA Kits) inhibitors.These findings expand our understanding of the components involved in head and neck squamous cell carcinoma autophagy machinery that responds to EGFR (show EGFR ELISA Kits) inhibitors.
TUFM is a novel regulator of epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)); there may be a molecular link between mitochondrial dysfunction and EMT (show ITK ELISA Kits) induction
NLRX1 (show NLRX1 ELISA Kits) and TUFM work in concert to reduce cytokine response and augment autophagy.
Increased expression of TUFM is a promising new prognostic indicator for colorectal carcinoma.
By recruiting Atg5 (show ATG5 ELISA Kits)-Atg12 (show ATG12 ELISA Kits) and NLRX1 (show NLRX1 ELISA Kits), TUFM serves as a nodal checkpoint of the RIG-I (show DDX58 ELISA Kits)-MAVS (show MAVS ELISA Kits) axis. It acts similarly to NLRX1 (show NLRX1 ELISA Kits) by inhibiting RigI (show DDX58 ELISA Kits)-like-receptor-induced IFN-I but promoting autophagy.
Genetic investigation of patients with defective mitochondrial translation led to the discovery of novel mutations in the mitochondrial elongation factor G1 (EFG1 (show GFM1 ELISA Kits)) in one affected baby and in the mitochondrial elongation factor Tu (show EEF1A1 ELISA Kits) (EFTu) in another one
Myoblasts isolated from the MELAS patients show A3243G mutation in tRNALeu(UUR) produces a severe respiratory chain deficiency and this phenotype can be partially suppressed by overexpression of EFTu and EFG2 (show GFM2 ELISA Kits).
Results suggest that the R336Q mutant mt-EFTu variant fails to bind to aminoacylated mitochondrial tRNAs, thus explaining the observed impairment of mitochondrial translation.
Loss of activity is caused by a significant reduction in the ability of EF-Ts(mt) R325W to bind EF-Tu(mt), leading to a defect in nucleotide exchange.
Recombinant mitochondrial EF-Tu prevents thermal aggregation of proteins and enhances protein refolding in vitro.
The arginine residue at position 335 of bovine mitochondrial elongation factor Tu (EF-Tu (show EEF1A1 ELISA Kits)) plays an important role in the binding and EF-Tu-mediated delivery of mitochondrial aminoacyl-tRNAs to the A-site of the ribosome.
This gene encodes a protein which participates in protein translation in mitochondria. Mutations in this gene have been associated with combined oxidative phosphorylation deficiency resulting in lactic acidosis and fatal encephalopathy. A pseudogene has been identified on chromosome 17.
Tu translation elongation factor, mitochondrial
, elongation factor Tu, mitochondrial-like
, elongation factor Tu, mitochondrial