2010
DOI: 10.1016/j.cellsig.2009.10.013
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A non-catalytic function of the Src family tyrosine kinases controls prolactin-induced Jak2 signaling

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Cited by 39 publications
(23 citation statements)
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“…It is important to note that the present study used a small molecule to very selectively inhibit Src kinase which is quite different from previous studies in which Src protein was depleted by siRNA, or inactivated by neutralizing antibodies or transfection of dominant negative Src. Here, KX-01 inhibits the kinase activity of Src although other functions of Src may be independent of its catalytic kinase activity as demonstrated by earlier studies using kinasedefective Src mutants [45]. Src protein may also function by recruiting other tyrosine kinases and such functions may be important in G1 regulation and would likely be unaffected by a pure kinase inhibitor [42].…”
Section: Discussionmentioning
confidence: 86%
“…It is important to note that the present study used a small molecule to very selectively inhibit Src kinase which is quite different from previous studies in which Src protein was depleted by siRNA, or inactivated by neutralizing antibodies or transfection of dominant negative Src. Here, KX-01 inhibits the kinase activity of Src although other functions of Src may be independent of its catalytic kinase activity as demonstrated by earlier studies using kinasedefective Src mutants [45]. Src protein may also function by recruiting other tyrosine kinases and such functions may be important in G1 regulation and would likely be unaffected by a pure kinase inhibitor [42].…”
Section: Discussionmentioning
confidence: 86%
“…Precedence for this hypothesis is based on literature describing the roles of effector proteins that alter signaling through this complex [34]. For example, c-Src has been shown to propagate PRL initiated JAK/STAT signaling in normal mammary tissue [35]. Additionally, caveolin-1 (Cav-1) has been shown to inhibit the STAT5 signaling pathway by competitively binding to the tyrosine kinase domain of JAK2, preventing interaction and subsequent activation of STAT5 [36].…”
Section: Discussionmentioning
confidence: 99%
“…Human cellular-Src (c-Src) is a second key signaling node for STAT5 activation in normal and malignant mammary epithelial cells. Loss of c-Src interrupts STAT5 activation during pregnancy, and in malignant cells c-Src has been shown to mediate STAT5 activation downstream of estrogen/estrogen receptor-alpha (ERα) and epidermal growth factor (EGF) signaling and to contribute to activation through the PRL/PRLR/JAK2 pathway [4,16,27-29]. One example of the impact of these interacting signaling nodes is shown by the dual activation of STAT5 by estrogen and EGF [28].…”
Section: Overview Of the Stat5 Signaling Node In Mammary Epithelial Cmentioning
confidence: 99%