◀ Back to BCL10

BCL10 — STAT5A

Text-mined interactions from Literome

Socolovsky et al., Cell 1999 (Anemia) : Fetal anemia and apoptosis of red cell progenitors in Stat5a-/-5b-/- mice : a direct role for Stat5 in Bcl-X ( L ) induction
Dumon et al., Oncogene 1999 : IL-3 dependent regulation of Bcl-xL gene expression by STAT5 in a bone marrow derived cell line
Lord et al., J Immunol 2000 : Proliferative signaling by a receptor mutant with a weak Stat5 activating site could be rescued by overexpression of wt Stat5a or b. Additionally, the ability of this receptor mutant to induce c-myc, bcl-x , and bcl-2 was enhanced by overexpression of wt Stat5
Gesbert et al., Blood 2000 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : The increase in transcription of the Bcl-X promoter and the increase in Bcl-X protein, due to p210 ( Bcr/Abl ), were blocked by expression of a dominant negative STAT5 mutant
Donato et al., Blood 2001 (Leukemia) : Expression of bcr-abl in interleukin-3 (IL-3)/granulocyte-macrophage colony stimulating factor ( GM-CSF ) -dependent Mo7e cells ( MBA ) resulted in growth factor independence, constitutive activation of Stat-5 phosphorylation, engagement of mitogen activated protein ( MAP ) kinase signals, and increased expression of PTP1B and bcl-x ( L )
Walton et al., Mech Dev 2001 : In erythroid cells bcl-x gene expression is controlled by cytokines and the transcription factor Stat5 ( signal transducer and activator of transcription )
Riedlinger et al., Biol Reprod 2002 : It has been proposed that Bcl-x is a key survival factor in many cell types, and that the bcl-x gene is activated by the transcription factor Stat5 through cytokine signals ... We have now investigated whether, in the mouse, Bcl-x is required for the postnatal maintenance of follicles and luteal cells, and whether Stat5 activates the bcl-x gene ... Furthermore, expression of the bcl-x gene in the ovary was independent of Stat5 and its activating hormone, prolactin
Morcinek et al., Oncogene 2002 : We identified STAT5 activation as being involved in both growth and survival signalling triggered by the Xmrk kinase possibly due to STAT5 induced expression of pim-1 and bcl-x
Versteeg et al., Circ Res 2004 : In conclusion, our results show that FVIIa induces cell survival through STAT5 dependent Bcl ( XL ) production and Jak2 dependent activation of PKB
Goetz et al., J Immunol 2005 : Thus, STAT5 dependent bcl-x ( L ) up-regulation and enhanced B cell survival are not sufficient to drive the thymic B cell development observed in STAT5b-CA mice
Qian et al., Biochim Biophys Acta 2009 (Glioma) : To determine whether Stat5 regulates Bcl-xL expression in CAM induced cell death, C6-glioma was infected with an adenovirus containing a constitutively activated Stat5-GFP ( Ad-Stat5ca ) ... Overexpression of Stat5ca increased Bcl-xL and decreased CAM induced cell death compared to control adenovirus infected cells ; whereas Stat5 siRNA decreased DX-induced Bcl-xL and increased cell death
Nagy et al., Molecular cancer 2009 (Lymphoma) : STAT5 regulation of BCL10 parallels constitutive NFkappaB activation in lymphoid tumor cells