BRENDA - Enzyme Database show

Hypoxia-induced deoxycytidine kinase expression contributes to apoptosis in chronic lung disease

Weng, T.; Karmouty-Quintana, H.; Garcia-Morales, L.J.; Molina, J.G.; Pedroza, M.; Bunge, R.R.; Bruckner, B.A.; Loebe, M.; Seethamraju, H.; Blackburn, M.R.; FASEB J. 27, 2013-2026 (2013)

Data extracted from this reference:

Cloned(Commentary)
EC Number
Commentary
Organism
2.7.1.74
quantitative RT-PCR expression analysis
Homo sapiens
2.7.1.74
quantitative RT-PCR expression analysis
Mus musculus
Engineering
EC Number
Amino acid exchange
Commentary
Organism
2.7.1.74
additional information
for enzyme knockout, MLE12 cells are transfected with DCK siRNA
Mus musculus
Organism
EC Number
Organism
Primary Accession No. (UniProt)
Commentary
Textmining
2.7.1.74
Homo sapiens
-
-
-
2.7.1.74
Mus musculus
-
Ada-/- mice
-
Source Tissue
EC Number
Source Tissue
Commentary
Organism
Textmining
2.7.1.74
MLE-12 cell
-
Mus musculus
-
2.7.1.74
pulmonary epithelial cell
-
Homo sapiens
-
2.7.1.74
pulmonary epithelial cell
-
Mus musculus
-
Substrates and Products (Substrate)
EC Number
Substrates
Commentary Substrates
Literature (Substrates)
Organism
Products
Commentary (Products)
Literature (Products)
Organism (Products)
Reversibility
2.7.1.74
NTP + deoxyadenosine
-
722221
Mus musculus
NDP + dAMP
-
-
-
?
2.7.1.74
NTP + deoxyadenosine
-
722221
Homo sapiens
NDP + dAMP
-
-
-
?
2.7.1.74
NTP + deoxycytidine
-
722221
Homo sapiens
NDP + dCMP
-
-
-
?
Cloned(Commentary) (protein specific)
EC Number
Commentary
Organism
2.7.1.74
quantitative RT-PCR expression analysis
Homo sapiens
2.7.1.74
quantitative RT-PCR expression analysis
Mus musculus
Engineering (protein specific)
EC Number
Amino acid exchange
Commentary
Organism
2.7.1.74
additional information
for enzyme knockout, MLE12 cells are transfected with DCK siRNA
Mus musculus
Source Tissue (protein specific)
EC Number
Source Tissue
Commentary
Organism
Textmining
2.7.1.74
MLE-12 cell
-
Mus musculus
-
2.7.1.74
pulmonary epithelial cell
-
Homo sapiens
-
2.7.1.74
pulmonary epithelial cell
-
Mus musculus
-
Substrates and Products (Substrate) (protein specific)
EC Number
Substrates
Commentary Substrates
Literature (Substrates)
Organism
Products
Commentary (Products)
Literature (Products)
Organism (Products)
Reversibility
2.7.1.74
NTP + deoxyadenosine
-
722221
Mus musculus
NDP + dAMP
-
-
-
?
2.7.1.74
NTP + deoxyadenosine
-
722221
Homo sapiens
NDP + dAMP
-
-
-
?
2.7.1.74
NTP + deoxycytidine
-
722221
Homo sapiens
NDP + dCMP
-
-
-
?
Expression
EC Number
Organism
Commentary
Expression
2.7.1.74
Homo sapiens
the enzyme is hypoxia-induced
up
2.7.1.74
Mus musculus
the enzyme is hypoxia-induced
up
General Information
EC Number
General Information
Commentary
Organism
2.7.1.74
malfunction
inhibition of the enzyme results in diminished dAdomediated apoptosis in the lungs
Homo sapiens
2.7.1.74
malfunction
inhibition of the enzyme results in diminished deoxyadenosine-mediated apoptosis in the lungs
Mus musculus
2.7.1.74
physiological function
deoxycitidine kinase is a major enzyme for deoxyadenosine phosphorylation. Hypoxia-induced deoxycytidine kinase expression contributes to apoptosis in chronic lung disease, hypoxia is a regulator of the enzyme
Homo sapiens
2.7.1.74
physiological function
deoxycitidine kinase is a major enzyme for deoxyadenosine phosphorylation. Hypoxia-induced deoxycytidine kinase expression contributes to apoptosis in chronic lung disease, hypoxia is a regulator of the enzyme. Activating the dAdo-DCK-dATP pathway directly results in increased apoptosis in the lungs of mice with air-space enlargement, the dAdo-DCK pathway is activated in the lungs of Ada-/- mice, overview
Mus musculus
General Information (protein specific)
EC Number
General Information
Commentary
Organism
2.7.1.74
malfunction
inhibition of the enzyme results in diminished dAdomediated apoptosis in the lungs
Homo sapiens
2.7.1.74
malfunction
inhibition of the enzyme results in diminished deoxyadenosine-mediated apoptosis in the lungs
Mus musculus
2.7.1.74
physiological function
deoxycitidine kinase is a major enzyme for deoxyadenosine phosphorylation. Hypoxia-induced deoxycytidine kinase expression contributes to apoptosis in chronic lung disease, hypoxia is a regulator of the enzyme
Homo sapiens
2.7.1.74
physiological function
deoxycitidine kinase is a major enzyme for deoxyadenosine phosphorylation. Hypoxia-induced deoxycytidine kinase expression contributes to apoptosis in chronic lung disease, hypoxia is a regulator of the enzyme. Activating the dAdo-DCK-dATP pathway directly results in increased apoptosis in the lungs of mice with air-space enlargement, the dAdo-DCK pathway is activated in the lungs of Ada-/- mice, overview
Mus musculus
Expression (protein specific)
EC Number
Organism
Commentary
Expression
2.7.1.74
Homo sapiens
the enzyme is hypoxia-induced
up
2.7.1.74
Mus musculus
the enzyme is hypoxia-induced
up