| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| The PIM 2 kinase phosphorylates BAD on serine 112 and reverses BAD induced cell death . ^^^ Our results indicate that pim 2 functions similarly to pim 1 as a pro survival kinase and suggest that BAD is a legitimate PIM 2 substrate . . ^^^ |
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| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| Pim kinases phosphorylate multiple sites on Bad and promote 14 3 3 binding and dissociation from Bcl XL . ^^^ RESULTS : Here we show that the pim kinases are constitutively active when expressed in HEK 293 cells and are able to phosphorylate the Bcl 2 family member Bad on three residues , Ser 112 , Ser 136 and Ser 155 in vitro and in cells . ^^^ Pim 3 was also able to phosphorylate other sites in Bad in vitro , including Ser 170 , another potential in vivo site . ^^^ Pim phosphorylation of Bad was also found to promote the 14 3 3 binding of Bad and block its association with Bcl XL . ^^^ CONCLUSION : All three Pim kinase family members predominantly phosphorylate Bad on Ser 112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro apoptotic function of Bad in HEK 293 cells . ^^^ |
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| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| Pim 3 , a proto oncogene with serine / threonine kinase activity , is aberrantly expressed in human pancreatic cancer and phosphorylates bad to block bad mediated apoptosis in human pancreatic cancer cell lines . ^^^ Moreover , Pim 3 mRNA and protein were constitutively expressed in all human pancreatic cancer cell lines that we examined and colocalized with the proapoptotic protein Bad . ^^^ Phosphorylation of Bad and the expression of an antiapoptotic molecule , Bcl 10 ( L ) , were reduced by the ablation of endogenous Pim 3 . ^^^ Thus , we provide the first evidence that Pim 3 can inactivate Bad and maintain the expression of Bcl 10 ( L ) and thus prevent apoptosis of human pancreatic cancer cells . ^^^ |
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| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| Pim 1 kinase promotes inactivation of the pro apoptotic Bad protein by phosphorylating it on the Ser 112 gatekeeper site . ^^^ Here , we show that Pim 1 colocalizes and physically interacts with the pro apoptotic Bad protein and phosphorylates it in vitro on serine 112 , which is a gatekeeper site for its inactivation . ^^^ Furthermore , wild type Pim 1 , but not a kinase deficient mutant , enhances phosphorylation of this site in FDCP 1 cells and protects cells from the pro apoptotic effects of Bad . ^^^ Our results suggest that phosphorylation of Bad by Pim 1 is one of several mechanisms via which the Pim 1 kinase can enhance Bcl 2 activity and promote cell survival . . ^^^ |
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| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| Western blot analysis indicated that KP 372 1 decreased the phosphorylation of AKT on both Ser ( 473 ) and Thr ( 308 ) ; abrogated the phosphorylation of p70S6 kinase , BAD , and Foxo3a via PI3K / AKT signaling ; and down regulated expression of PIM 1 through direct inhibition of FLT 3 . ^^^ |
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| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| Constitutively activated FLT 3 phosphorylates BAD partially through pim 1 . ^^^ Upstream proteins known to phosphorylate BAD include Akt , extracellular signal regulated kinase / mitogen activated protein kinase ( Erk / MAPK ) , Pim 1 and Pim 2 . ^^^ Our data suggests that Pim 1 is one of the principal kinases mediating the anti apoptotic function of FLT3 / ITD signalling via the phosphorylation of BAD . . ^^^ |
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| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P11309 and Q92934 |
Pubmed |
SVM Score :0.0 |
| NA |
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