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Literature summary 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

EC Number Protein Variants Comment Organism
2.7.10.2 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
2.7.10.2 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

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

Natural Substrates/ Products (Substrates)

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

Organism

EC Number Organism UniProt Comment Textmining
2.7.10.2 Homo sapiens
-
-
-
2.7.10.2 Mus musculus
-
-
-

Substrates and Products (Substrate)

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

Synonyms

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

Cofactor

EC Number Cofactor Comment Organism Structure
2.7.10.2 ATP
-
 Mus musculus
2.7.10.2 ATP
-
 Homo sapiens

General Information

EC Number General Information Comment Organism
2.7.10.2 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
2.7.10.2 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