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Literature summary for 3.4.21.79 extracted from

  • Batinac, T.; Zamolo, G.; Coklo, M.; Hadzisejdic, I.
    Possible key role of granzyme B in keratoacanthoma regression (2006), Med. Hypotheses, 66, 1129-1132.
    View publication on PubMed
Search for more literature for 3.4.21.79

Application

Application Comment Organism
medicine key role of plasticity in the granzyme B mediated cell death pathway in the killing of changed tumor cells, resulting in keratoacanthoma regression through apoptosis or direct damage of tumor cells. Insufficient activation of cytotoxic T lymphocytes and decreased release or activity of granzyme B may be responsible for squamous cell-carcinoma progression and occasional aggressive behavior in keratoacanthomas. Targeted delivery of granzyme B to squamous cell, carcinoma cells may be a new agent that may have an additive or synergic effect with conventional therapeutic modalities, since there are still no known cellular resistance mechanisms capable of protecting cells against all granzyme B mediated pathways Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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-
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Source Tissue

Source Tissue Comment Organism Textmining
cytotoxic T-lymphocyte cell line
-
 Homo sapiens
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skin
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 Homo sapiens
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
BID + H2O
-
 Homo sapiens truncated BID + ?
-
 ?
pro-caspase-3 + H2O
-
 Homo sapiens caspase-3 + ?
-
 ?
procaspase-8 + H2O
-
 Homo sapiens caspase-8 + ?
-
 ?