Gene interactions and pathways from curated databases and text-mining

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JAK2 — PIK3R1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Krasilnikov et al., Oncogene 2003 (Melanoma) : Tyrosine phosphorylation of STAT3/5 and of JAK2 also increased upon treatment of LU1205 cells with either PD or LY, suggesting that constitutive active MAPK and PI3K signals inhibit tyrosine phosphorylation of JAK/STATs
Choudhury et al., Metabolism 2006 : These effects were blocked by JAK2 inhibition as well as PI3K inhibition
Naito et al., Nagoya J Med Sci 2005 : AG-490, a Jak-2 inhibitor, or LY294002, a PI3K inhibitor , similarly suppressed the augmented production of hyarulonan
Luo et al., Eur J Neurosci 2007 (Optic Nerve Injuries) : In this study we showed that : ( i ) the RGC protection was pathway inhibition dependent ; ( ii ) inhibition of PI3K/akt and JAK/STAT , but not MEK/ERK, activated macrophages in the eye, ( iii ) macrophage removal from the eye using clodronate liposomes significantly impeded PI3K/akt and JAK/STAT inhibition induced RGC survival and axon regeneration whereas it only slightly affected MEK/ERK inhibition dependent protection ; ( iv ) in the absence of recruited macrophages in the eye, inhibition of PI3K/akt or JAK/STAT did not influence RGC survival ; and ( v ) strong PI3K/akt , JAK/STAT and MEK/ERK pathway activities were located in RGCs but not macrophages after ON injury
Huang et al., J Immunol 2007 : Requirement for both JAK mediated PI3K signaling and ACT1/TRAF6/TAK1 dependent NF-kappaB activation by IL-17A in enhancing cytokine expression in human airway epithelial cells
Lin et al., Toxicol In Vitro 2010 (Breast Neoplasms) : Moreover, the JAK2 inhibitor AG490 blocked JAK2, STAT3, Src, PI3K, and Akt activation, whereas both Src inhibitor PP2 and PI3K inhibitor wortmannin did not affect JAK2 activation
Su et al., Clin Exp Pharmacol Physiol 2010 : These observations suggest that PI3-K is an upstream activator of JAK2/STAT3
Li et al., PloS one 2012 (Hypereosinophilic Syndrome) : Interestingly, JAK2 inhibition also reduced PI3K , Akt and NF-?B activity in a dose dependent manner, and suppressed expression levels of c-Myc and Survivin ... Interestingly, JAK2 inhibition also reduced PI3K , Akt and NF-?B activity in a dose dependent manner, and suppressed expression levels of c-Myc and Survivin
Chang et al., Gen Comp Endocrinol 2012 : The specific inhibitors of either MEK1 ( U-0126 and PD-98059 ), JAK ( AG-490 ), JNK ( SP-600125 ), or PI3K ( LY-294002 and wortmannin ) reduced ET-1 increased levels of SOCS-3 mRNA and respectively inhibited ET-1 stimulated activities of MEK1, JAK, JNK, and PI3K
Britschgi et al., Cancer Cell 2012 (Breast Neoplasms...) : Mechanistically, PI3K/mTOR inhibition increased IRS1 dependent activation of JAK2/STAT5 and secretion of IL-8 in several cell lines and primary breast tumors