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Literature summary for 2.7.10.2 extracted from

  • Ghoreschi, K.; Laurence, A.; OShea, J.J.
    Janus kinases in immune cell signaling (2009), Immunol. Rev., 228, 273-287.
    View publication on PubMedView publication on EuropePMC

Protein Variants

Protein Variants Comment Organism
V617F the mutation within the JH2 pseudokinase domain of Jak2 is present in almost all patients with polycythemia vera, as well as high percentages also in patients with essential thrombocythemia, and idiopathic myelofibrosis Mus musculus
V617F the mutation within the JH2 pseudokinase domain of Jak2 is present in almost all patients with polycythemia vera, as well as high percentages also in patients with essential thrombocythemia, and idiopathic myelofibrosis Homo sapiens

Inhibitors

Inhibitors Comment Organism Structure
CP-690 550 Jak3 and Jak2 inhibitor Homo sapiens
CP-690 550 Jak3 and Jak2 inhibitor Mus musculus
dasatinib Jak2 inhibitor, at high doses (0.001 mM), dasatinib can inhibit Jak2 activity in vitro Homo sapiens
dasatinib Jak2 inhibitor, at high doses (0.001 mM), dasatinib can inhibit Jak2 activity in vitro Mus musculus
INCB018424 Jak2 inhibitor Homo sapiens
INCB018424 Jak2 inhibitor Mus musculus
lestaurtinib Jak2 inhibitor Homo sapiens
lestaurtinib Jak2 inhibitor Mus musculus
PNU156804 Jak3 inhibitor Homo sapiens
PNU156804 Jak3 inhibitor Mus musculus
SB1518 Jak2 inhibitor Homo sapiens
SB1518 Jak2 inhibitor Mus musculus
TG101348 Jak2 inhibitor Homo sapiens
TG101348 Jak2 inhibitor Mus musculus
tyrphostin AG490 Jak3 inhibitor Homo sapiens
tyrphostin AG490 Jak3 inhibitor Mus musculus
WHI-P131 Jak3 inhibitor Homo sapiens
WHI-P131 Jak3 inhibitor Mus musculus
WHI-P154 Jak3 inhibitor Homo sapiens
WHI-P154 Jak3 inhibitor Mus musculus

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + a [protein]-L-tyrosine Mus musculus
-
ADP + a [protein]-L-tyrosine phosphate
-
?
ATP + a [protein]-L-tyrosine Homo sapiens
-
ADP + a [protein]-L-tyrosine phosphate
-
?

Organism

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

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + a [protein]-L-tyrosine
-
Mus musculus ADP + a [protein]-L-tyrosine phosphate
-
?
ATP + a [protein]-L-tyrosine
-
Homo sapiens ADP + a [protein]-L-tyrosine phosphate
-
?

Synonyms

Synonyms Comment Organism
Jak1
-
Mus musculus
Jak1
-
Homo sapiens
JAK2
-
Mus musculus
JAK2
-
Homo sapiens
Jak3
-
Mus musculus
Jak3
-
Homo sapiens
Janus kinase
-
Mus musculus
Janus kinase
-
Homo sapiens
non-receptor protein tyrosine kinase
-
Mus musculus
non-receptor protein tyrosine kinase
-
Homo sapiens
Tyk2
-
Mus musculus
Tyk2
-
Homo sapiens

Cofactor

Cofactor Comment Organism Structure
ATP
-
Mus musculus
ATP
-
Homo sapiens

General Information

General Information Comment Organism
malfunction deficiency of Jak3 or Tyk2 results in defined clinical disorders, a striking phenotype associated with inactivating Jak3 mutations is severe combined immunodeficiency syndrome, whereas mutation of Tyk2 results in autosomal recessive hyperimmunoglobulin E syndrome, complete deletion of Jak1 or Jak2 in the mouse are not compatible with life and do not have counterparts in human disease. Activating mutations of each of the Jaks are found in association with malignant transformation, the most common being gain-of-function mutations of Jak2 in polycythemia vera and other myeloproliferative disorders. Homo sapiens
malfunction deficiency of Jak3 or Tyk2 results in defined clinical disorders, a striking phenotype associated with inactivating Jak3 mutations is severe combined immunodeficiency syndrome, whereas mutation of Tyk2 results in autosomal recessive hyperimmunoglobulin E syndrome, complete deletion of Jak1 or Jak2 in the mouse are not compatible with life and do not have counterparts in human disease. Activating mutations of each of the Jaks are found in association with malignant transformation, the most common being gain-of-function mutations of Jak2 in polycythemia vera and other myeloproliferative disorders. Jak1 knockout mice have major deficits in lymphopoiesis and a failure to respond to signals from class II cytokine receptors, gammac cytokine receptors, and cytokine receptors that contain the gp130 subunit. Jak2 deficiency is lethal. Mus musculus