Sort by
Items per page

Send to

Choose Destination

Links from PubMed

Items: 1 to 20 of 248


The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenes.

Wernig G, Gonneville JR, Crowley BJ, Rodrigues MS, Reddy MM, Hudon HE, Walz C, Reiter A, Podar K, Royer Y, Constantinescu SN, Tomasson MH, Griffin JD, Gilliland DG, Sattler M.

Blood. 2008 Apr 1;111(7):3751-9. doi: 10.1182/blood-2007-07-102186.


STAT5 activation is critical for the transformation mediated by myeloproliferative disorder-associated JAK2 V617F mutant.

Funakoshi-Tago M, Tago K, Abe M, Sonoda Y, Kasahara T.

J Biol Chem. 2010 Feb 19;285(8):5296-307. doi: 10.1074/jbc.M109.040733.


Induction of tyrosine phosphorylation of Vav and expression of Pim-1 correlates with Jak2-mediated growth signaling from the erythropoietin receptor.

Miura O, Miura Y, Nakamura N, Quelle FW, Witthuhn BA, Ihle JN, Aoki N.

Blood. 1994 Dec 15;84(12):4135-41.


Tyrosine 201 is required for constitutive activation of JAK2V617F and efficient induction of myeloproliferative disease in mice.

Yan D, Hutchison RE, Mohi G.

Blood. 2012 Aug 30;120(9):1888-98. doi: 10.1182/blood-2011-09-380808.


Activated Jak2 with the V617F point mutation promotes G1/S phase transition.

Walz C, Crowley BJ, Hudon HE, Gramlich JL, Neuberg DS, Podar K, Griffin JD, Sattler M.

J Biol Chem. 2006 Jun 30;281(26):18177-83.


Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation.

Lu X, Levine R, Tong W, Wernig G, Pikman Y, Zarnegar S, Gilliland DG, Lodish H.

Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18962-7.


Dimerization by a cytokine receptor is necessary for constitutive activation of JAK2V617F.

Lu X, Huang LJ, Lodish HF.

J Biol Chem. 2008 Feb 29;283(9):5258-66.


Akt activation through the phosphorylation of erythropoietin receptor at tyrosine 479 is required for myeloproliferative disorder-associated JAK2 V617F mutant-induced cellular transformation.

Kamishimoto J, Tago K, Kasahara T, Funakoshi-Tago M.

Cell Signal. 2011 May;23(5):849-56. doi: 10.1016/j.cellsig.2011.01.009.


Critical roles of Myc-ODC axis in the cellular transformation induced by myeloproliferative neoplasm-associated JAK2 V617F mutant.

Funakoshi-Tago M, Sumi K, Kasahara T, Tago K.

PLoS One. 2013;8(1):e52844. doi: 10.1371/journal.pone.0052844.


Targeting PIM kinases impairs survival of hematopoietic cells transformed by kinase inhibitor-sensitive and kinase inhibitor-resistant forms of Fms-like tyrosine kinase 3 and BCR/ABL.

Adam M, Pogacic V, Bendit M, Chappuis R, Nawijn MC, Duyster J, Fox CJ, Thompson CB, Cools J, Schwaller J.

Cancer Res. 2006 Apr 1;66(7):3828-35.


The PIM inhibitor AZD1208 synergizes with ruxolitinib to induce apoptosis of ruxolitinib sensitive and resistant JAK2-V617F-driven cells and inhibit colony formation of primary MPN cells.

Mazzacurati L, Lambert QT, Pradhan A, Griner LN, Huszar D, Reuther GW.

Oncotarget. 2015 Nov 24;6(37):40141-57. doi: 10.18632/oncotarget.5653.


[Analysis of the mechanism of polycythemia vera by studying JAK2 mutant-induced signaling pathway].

Funakoshi-Tago M.

Yakugaku Zasshi. 2011;131(8):1183-7. Review. Japanese.


SOCS2: inhibitor of JAK2V617F-mediated signal transduction.

Quentmeier H, Geffers R, Jost E, Macleod RA, Nagel S, Röhrs S, Romani J, Scherr M, Zaborski M, Drexler HG.

Leukemia. 2008 Dec;22(12):2169-75. doi: 10.1038/leu.2008.226.


Conditional expression of heterozygous or homozygous Jak2V617F from its endogenous promoter induces a polycythemia vera-like disease.

Akada H, Yan D, Zou H, Fiering S, Hutchison RE, Mohi MG.

Blood. 2010 Apr 29;115(17):3589-97. doi: 10.1182/blood-2009-04-215848.


MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia.

Pikman Y, Lee BH, Mercher T, McDowell E, Ebert BL, Gozo M, Cuker A, Wernig G, Moore S, Galinsky I, DeAngelo DJ, Clark JJ, Lee SJ, Golub TR, Wadleigh M, Gilliland DG, Levine RL.

PLoS Med. 2006 Jul;3(7):e270.


Erythropoietin induces activation of Stat5 through association with specific tyrosines on the receptor that are not required for a mitogenic response.

Quelle FW, Wang D, Nosaka T, Thierfelder WE, Stravopodis D, Weinstein Y, Ihle JN.

Mol Cell Biol. 1996 Apr;16(4):1622-31.


Lyn physically associates with the erythropoietin receptor and may play a role in activation of the Stat5 pathway.

Chin H, Arai A, Wakao H, Kamiyama R, Miyasaka N, Miura O.

Blood. 1998 May 15;91(10):3734-45.

Supplemental Content

Support Center