Nerve growth factor-induced differentiation of PC12 cells employs the PMA-insensitive protein kinase C-ζ isoform

1994 ◽  
Vol 5 (1) ◽  
pp. 39-57 ◽  
Author(s):  
Elaine S. Coleman ◽  
Marie W. Wooten
Keyword(s):  
Protein Kinase C ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Induced Differentiation ◽  
Nerve Growth ◽  
Kinase C

Nerve growth factor enhances the level of the protein kinase C substrate B-50 in pheochromocytoma PC12 cells

1986 ◽  
Vol 139 (2) ◽  
pp. 644-651 ◽  
Author(s):  
C.O.M. Van Hooff ◽  
P.N.E. De Graan ◽  
J. Boonstra ◽  
A.B. Oestreicher ◽  
M.H. Schmidt-Michels ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Nerve Growth ◽  
Kinase C ◽  
Pheochromocytoma Pc12 ◽  
Pheochromocytoma Pc12 Cells

scholarly journals Nerve growth factor stimulates protein kinase C translocation in PC12 cells

FEBS Letters ◽  
1990 ◽  
Vol 264 (1) ◽  
pp. 75-77 ◽  
Author(s):  
A.D. Kondratyev ◽  
O.N. Popova ◽  
S.E. Severin ◽  
M.A. Choladze ◽  
I.I. Shmyrev ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Nerve Growth ◽  
Kinase C

scholarly journals Nerve growth factor-induced changes in the intracellular localization of the protein kinase C substrate B-50 in pheochromocytoma PC12 cells.

1989 ◽  
Vol 108 (3) ◽  
pp. 1115-1125 ◽  
Author(s):  
C O Van Hooff ◽  
J C Holthuis ◽  
A B Oestreicher ◽  
J Boonstra ◽  
P N De Graan ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Protein Kinase C ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Plasma Membranes ◽  
Nerve Growth ◽  
Kinase C ◽  
Pheochromocytoma Pc12

High levels of the neuron-specific protein kinase C substrate, B-50 (= GAP43), are present in neurites and growth cones during neuronal development and regeneration. This suggests a hitherto nonelucidated role of this protein in neurite outgrowth. Comparable high levels of B-50 arise in the pheochromocytoma PC12 cell line during neurite formation. To get insight in the putative growth-associated function of B-50, we compared its ultrastructural localization in naive PC12 cells with its distribution in nerve growth factor (NGF)- or dibutyryl cyclic AMP (dbcAMP)-treated PC12 cells. B-50 immunogold labeling of cryosections of untreated PC12 cells is mainly associated with lysosomal structures, including multivesicular bodies, secondary lysosomes, and Golgi apparatus. The plasma membrane is virtually devoid of label. However, after 48-h NGF treatment of the cells, B-50 immunoreactivity is most pronounced on the plasma membrane. Highest B-50 immunoreactivity is observed on plasma membranes surrounding sprouting microvilli, lamellipodia, and filopodia. Outgrowing neurites are scattered with B-50 labeling, which is partially associated with chromaffin granules. In NGF-differentiated PC12 cells, B-50 immunoreactivity is, as in untreated cells, also associated with organelles of the lysosomal family and Golgi stacks. B-50 distribution in dbcAMP-differentiated cells closely resembles that in NGF-treated cells. The altered distribution of B-50 immunoreactivity induced by differentiating agents indicates a shift of the B-50 protein towards the plasma membrane. This translocation accompanies the acquisition of neuronal features of PC12 cells and points to a neurite growth-associated role for B-50, performed at the plasma membrane at the site of protrusion.

scholarly journals Mapping of Atypical Protein Kinase C within the Nerve Growth Factor Signaling Cascade: Relationship to Differentiation and Survival of PC12 Cells

2000 ◽  
Vol 20 (13) ◽  
pp. 4494-4504 ◽  
Author(s):  
Marie W. Wooten ◽  
M. Lamar Seibenhener ◽  
Kimberly B. W. Neidigh ◽  
Michel L. Vandenplas
Keyword(s):  
Protein Kinase C ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Dominant Negative ◽  
Atypical Protein Kinase C ◽  
Nerve Growth ◽  
Atypical Protein Kinase ◽  
Kinase C

ABSTRACT The pathway by which atypical protein kinase C (aPKC) contributes to nerve growth factor (NGF) signaling is poorly understood. We previously reported that in PC12 cells NGF-induced activation of mitogen-activated protein kinase (MAPK) occurs independently of classical and nonclassical PKC isoforms, whereas aPKC isoforms were shown to be required for NGF-induced differentiation. NGF-induced activation of PKC-ι was observed to be dependent on phosphatidylinositol 3-kinase (PI3K) and led to coassociation of PKC-ι with Ras and Src. Expression of dominant negative mutants of either Src (DN2) or Ras (Asn-17) impaired activation of PKC-ι by NGF. At the level of Raf-1, neither PKC-ι nor PI3 kinase was required for activation; however, PKC-ι could weakly activate MEK. Inhibitors of PKC-ι activity and PI3K had no effect on NGF-induced MAPK or p38 activation but reduced NGF-stimulated c-Jun N-terminal kinase activity. Src, PI3K, and PKC-ι were likewise required for NGF-induced NF-κB activation and cell survival, whereas Ras was not required for either survival or NF-κB activation but was required for differentiation. IKK existed as a complex with PKC-ι, Src and IκB. Consistent with a role for Src in regulating NF-κB activation, an absence of Src activity impaired recruitment of PKC-ι into an IKK complex and markedly impaired NGF-induced translocation of p65/NF-κB to the nucleus. These findings reveal that in PC12 cells, aPKCs comprise a molecular switch to regulate differentiation and survival responses coupled downstream to NF-κB. On the basis of these findings, Src emerges as a critical upstream regulator of both PKC-ι and the NF-κB pathway.

Sign in / Sign up

Export Citation Format

Share Document