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Literature summary for 3.1.2.22 extracted from

  • Tardy, C.; Sabourdy, F.; Garcia, V.; Jalanko, A.; Therville, N.; Levade, T.; Andrieu-Abadie, N.
    Palmitoyl protein thioesterase 1 modulates tumor necrosis factor alpha-induced apoptosis (2009), Biochim. Biophys. Acta, 1793, 1250-1258.
    View publication on PubMed
Search for more literature for 3.1.2.22

Cloned(Commentary)

Cloned (Comment) Organism
PPT1-deficient fibroblasts stably transfected with cDNA encoding PPT1 Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P50897
-
-
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
fibroblast normal fibroblasts and infantile neuronal ceroid lipofuscinosis fibroblasts, deficient of PPT1 Homo sapiens
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additional information Ppt1/Cln1-deficient cells Mus musculus
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
4-methylumbelliferyl 6-S-palmitoyl-6-thio-beta-D-glucoside + H2O
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 Mus musculus 4-methylumbelliferyl 6-thio-beta-D-glucoside + palmitate
-
 ?
4-methylumbelliferyl 6-S-palmitoyl-6-thio-beta-D-glucoside + H2O
-
 Homo sapiens 4-methylumbelliferyl 6-thio-beta-D-glucoside + palmitate
-
 ?

Synonyms

Synonyms Comment Organism
palmitoyl protein thioesterase 1
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 Mus musculus
palmitoyl protein thioesterase 1
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 Homo sapiens
PPT1
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 Mus musculus
PPT1
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction PPT1 deficient cells are partially resistant to tumor necrosis factor-induced cell death (57-75% cell viability versus 15-30% for control fibroblasts), tumor necrosis factor-initiated proteolytic cleavage of caspase-8, Bid and caspase-3, as well as cytochrome c release is strongly attenuated. Activation of p42/p44 mitogen-activated protein kinase and of transcription factor NF-kappaB by tumor necrosis factor, and induction of cell death by staurosporine or chemotherapeutic drugs in infantile neuronal ceroid lipofuscinosis cells are unaffected by PPT1 deficiency Homo sapiens
malfunction resistance to tumor necrosis factor-induced apoptosis in embryonic fibroblasts derived from Ppt1/Cln1-deficient mice but not from mice with a targeted deletion of Cln3 or Cln5 (murine models of ceroid lipofuscinosis) Mus musculus
physiological function role of PPT1 and, likely, protein depalmitoylation in the regulation of tumor necrosis factor-induced apoptosis Mus musculus
physiological function role of PPT1 and, likely, protein depalmitoylation in the regulation of tumor necrosis factor-induced apoptosis. PPT1 is involved in cell death triggered by death receptors but not receptor-independent cytotoxic agents. Expression of PPT1 cDNA in infantile neuronal ceroid lipofuscinosis cells restores the tumor necrosis factor sensitivity Homo sapiens