What question did this study set out to answer?

To determine how hematopoietic growth factors and bryostatin-1 regulate BCL2 alpha phosphorylation and protect myeloid cells from apoptosis.

October 1, 1994Journal of Biological ChemistryOpen Access

Interleukin-3 and bryostatin-1 mediate hyperphosphorylation of BCL2 alpha in association with suppression of apoptosis.

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Authors

WMW. Stratford MayResearch Triangle Park Foundation PTP G TylerJohns Hopkins University TITakahiko ItoThe Cancer Institute Hospital

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Implication

In vitro study reveals that interleukin-3 and bryostatin-1 suppress apoptosis via PKC-mediated BCL2 alpha phosphorylation in myeloid cells, highlighting a key role for classic PKC isoforms.

Key Points

To determine how hematopoietic growth factors and bryostatin-1 regulate BCL2 alpha phosphorylation and protect myeloid cells from apoptosis.
Treated murine myeloid factor-dependent FDC-P1/ER cells and recombinant BCL2 alpha-expressing NFS/N1.H-7 cells with interleukin-3, erythropoietin, or bryostatin-1.
Assessed cell survival and BCL2 alpha phosphorylation in the presence of PKC inhibitors (H-7, staurosporine) versus a PKA inhibitor (HA1004).
Conducted in vitro Ca2+-dependent kinase assays using purified PKC and performed comparative phosphopeptide mapping against intact cellular BCL2 alpha.
Interleukin-3, erythropoietin, and bryostatin-1 induced rapid serine phosphorylation of BCL2 alpha and suppressed apoptosis in growth factor-dependent cells.
Pharmacological inhibition of PKC by H-7 and staurosporine, but not PKA inhibition by HA1004, blocked both BCL2 alpha hyperphosphorylation and anti-apoptotic protection.
Purified PKC directly mediated Ca2+-dependent phosphorylation of BCL2 alpha in vitro on serine residues identical to those targeted during in vivo agonist treatment.

Cite This Study

May et al. (1994) studied this question.

synapsesocial.com/papers/6a72c18a8031ec7bb1dd7870 https://doi.org/10.1016/s0021-9258(18)47099-8

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Implication

In vitro study reveals that interleukin-3 and bryostatin-1 suppress apoptosis via PKC-mediated BCL2 alpha phosphorylation in myeloid cells, highlighting a key role for classic PKC isoforms.

Interleukin-3 and bryostatin-1 mediate hyperphosphorylation of BCL2 alpha in association with suppression of apoptosis.

Discussion

Member takes

Implication

Key Points

Cite This Study

Interleukin-3 and bryostatin-1 mediate hyperphosphorylation of BCL2 alpha in association with suppression of apoptosis.

Discussion

Member takes

Implication

Key Points

Cite This Study

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