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Severe deficiency of thymidine kinase (zeige TK1 ELISA Kits) 2 was associated with patients with mild forms of myopathy.
Data indicate that the thymidine kinase (zeige TK1 ELISA Kits) 2 enzyme kinetics of thymidine (dT) phosphorylation exhibits negative cooperativity, but deoxycytidine (dC) phosphorylation follows hyperbolic Michaelis-Menten kinetics.
thymidine kinase (zeige TK1 ELISA Kits) 2 but not deoxyguanosine kinase (zeige DGUOK ELISA Kits) is up-regulated during the stationary growth phase of cultured cells
We suggest that a chip including DPYD (zeige DPYD ELISA Kits), TYMS (zeige TYMS ELISA Kits), TYMP (zeige TYMP ELISA Kits), TK1 (zeige TK1 ELISA Kits), and TK2 (zeige TK1 ELISA Kits) genes is a potential tool to predict response in LARC (zeige CCL20 ELISA Kits) following fluoropyrimidine-based CCRT.
Clinically, hypotonia and proximal muscle weakness are the major phenotypes present in all subjects. In summary, our study expands the molecular and clinical spectrum associated with TK2 deficiency.
Thymidine kinase (zeige TK1 ELISA Kits)-2 mutations causing mtDNA deletions are linked to a case of late-onset respiratory failure.
Results strongly suggest that oxidative damage-induced S-glutathionylation and degradation of TK2 have significant impact on mitochondrial DNA precursor synthesis.
R225W and T230A mutation of TK2 leads to a significant reduction activity in autosomal recessive progressive external ophthalmoplegia patients.
TK2-deficient cells showed severe mtDNA depletion.
TK2 mutations have been identified in four patients from two families with myopathic mitochondrial DNA depletion and spinal muscular atrophy.
Data indicate that long term Dm-dNK ( nucleoside kinase from Drosophila melanogaster) expression rescued thymidine kinase 2 (Tk2)-deficient mice without lethal side effects.
Thymidine kinase (zeige TK1 ELISA Kits) 2 deficiency-induced mtDNA depletion in mouse liver leads to defect beta-oxidation.
TK2 deficiency disturbs myogenic progenitor cells function in postnatal skeletal muscle
analysis of transcripts encoding up to fourteen components of specific adipose tissue functions revealed that, in both TK2-deficient WAT and BAT (zeige BAAT ELISA Kits), there was a consistent reduction of thermogenesis related gene expression and severe reduction in leptin (zeige LEP ELISA Kits) mRNA
The down-regulation of Tk1 activity unmasks Tk2 deficiency in Tk2-/- mice and correlates with the onset of mtDNA depletion in the brain and the heart.
blood cells are less dependent on mitochondrial Tk2 compared with several other tissues; these cells can synthesize deoxyribonucleotides required for mtDNA replication by alternative pathways such as phosphorylation of thymidine by cytosolic Tk1 (zeige TK1 ELISA Kits)
Loss of TK2 activity leads to a severe ataxic phenotype, accompanied by reduced mtDNA copy number and decreased steady-state levels of electron transport chain proteins in the brain.
Tk2 has a major role in supplying deoxyribonucleotides for mtDNA replication and other pathways of deoxyribonucleotide synthesis cannot compensate for loss of this enzyme.
Tk2(-/-) animals showed Tk2 deficiency, unbalanced dNTP pools, mtDNA depletion and defects of respiratory chain enzymes.
This gene encodes a deoxyribonucleoside kinase that specifically phosphorylates thymidine, deoxycytidine, and deoxyuridine. The encoded enzyme localizes to the mitochondria and is required for mitochondrial DNA synthesis. Mutations in this gene are associated with a myopathic form of mitochondrial DNA depletion syndrome. Alternate splicing results in multiple transcript variants encoding distinct isoforms, some of which lack transit peptide, so are not localized to mitochondria.
, TK 2
, transketolase-like protein 1
, transketolase-related protein
, transketolase 2
, thymidine kinase 2, mitochondrial
, putative deoxyribonucleoside kinase
, thymidine kinase 2, mitochondrial S homeolog