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Literature summary for 3.4.21.38 extracted from

  • Jablonska, E.; Markart, P.; Zakrzewicz, D.; Preissner, K.T.; Wygrecka, M.
    Transforming growth factor-beta1 induces expression of human coagulation factor XII via Smad3 and JNK signaling pathways in human lung fibroblasts (2010), J. Biol. Chem., 285, 11638-11651.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.21.38

Activating Compound

Activating Compound Comment Organism Structure
TGFbeta treatment of human lung fibroblasts with TGF-beta1 results in a time-dependent increase in FXII production, activation of p44/42, p38, JNK, and Akt, and phosphorylation and translocation into the nucleus of Smad3 Homo sapiens

Cloned(Commentary)

Cloned (Comment) Organism
the FXII promoter contains the -299/+1 region, that is sufficient for TGF-beta1 to induce FXII expression Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
additional information Homo sapiens coagulation factor XII is a liver-derived serine protease involved in fibrinolysis, coagulation, and inflammation, regulation of FXII expression by TGF-beta-1, a multifunctional cytokine, overview ?
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 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
fibroblast
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 Homo sapiens
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liver
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 Homo sapiens
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lung
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 Homo sapiens
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
additional information coagulation factor XII is a liver-derived serine protease involved in fibrinolysis, coagulation, and inflammation, regulation of FXII expression by TGF-beta-1, a multifunctional cytokine, overview Homo sapiens ?
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 ?

Synonyms

Synonyms Comment Organism
coagulation factor XII
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 Homo sapiens
FXII
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 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens transforming growth factor-beta1, TGF-beta1, a multifunctional cytokine, induces FXII expression, which is specifically repressed by the JNK inhibitor, and by JNK and Smad3 antisense oligonucleotides, but not by MEK, p38, or phosphoinositide 3-kinase blockers, overview. Treatment of human lung fibroblasts with TGF-beta1 results in a time-dependent increase in FXII production, activation of p44/42, p38, JNK, and Akt, and phosphorylation and translocation into the nucleus of Smad3. The FXII promoter contains the -299/+1 region, that is sufficient for TGF-beta1 to induce FXII expression, but the activation of FXII expression also requires Smad binding to TGF-beta1 at the a potential Smad binding element at position -272/-269 (SBE-(-272/-269)) of the TGF-beta1 promoter. JNK/Smad3 pathway plays a critical role in TGF-beta1-induced FXII expression in human lung fibroblasts up

General Information

General Information Comment Organism
malfunction the JNK/Smad3 pathway plays a critical role in TGF-beta1-induced FXII expression in human lung fibroblasts implicating its possible involvement in pathological conditions characterized by elevated TGF-beta1 levels Homo sapiens
physiological function coagulation factor XII is a liver-derived serine protease involved in fibrinolysis, coagulation, and inflammation Homo sapiens