Evidence map›Paper›PMID 10848576›Full record

ArticleMolecular and cellular biology2000

Mapping of atypical protein kinase C within the nerve growth factor signaling cascade: relationship to differentiation and survival of PC12 cells.

M W Wooten, M L Seibenhener, K B Neidigh, M L Vandenplas

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 72 citations in OpenAlex.

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  12. IkappaB kinase beta phosphorylates Dok1 serines in response to TNF, IL-1, or gamma radiation.Proceedings of the National Academy of Sciences of the United States of America · 2004
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

M W WootenDepartment of Biological Sciences, Program in Cell and Molecular Biosciences, Auburn University, AL 36849, USA. mwwooten@ag.auburn.edu
M L Seibenhener
K B Neidigh
M L Vandenplas
Auburn University · US

Funding

NERVE GROWTH FACTOR SIGNALLINGR01NS033661 · NINDS · AUBURN UNIVERSITY AT AUBURN · PI WOOTEN, MICHAEL C · 1995 to 2013
$2.7M
NINDS NIH HHS R01 NS033661NINDS NIH HHS R02-NS33661
6 · The paper itself

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-iota was observed to be dependent on phosphatidylinositol 3-kinase (PI3K) and led to coassociation of PKC-iota with Ras and Src. Expression of dominant negative mutants of either Src (DN2) or Ras (Asn-17) impaired activation of PKC-iota by NGF. At the level of Raf-1, neither PKC-iota nor PI3 kinase was required for activation; however, PKC-iota could weakly activate MEK. Inhibitors of PKC-iota 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-iota were likewise required for NGF-induced NF-kappaB activation and cell survival, whereas Ras was not required for either survival or NF-kappaB activation but was required for differentiation. IKK existed as a complex with PKC-iota, Src and IkappaB. Consistent with a role for Src in regulating NF-kappaB activation, an absence of Src activity impaired recruitment of PKC-iota into an IKK complex and markedly impaired NGF-induced translocation of p65/NF-kappaB 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-kappaB. On the basis of these findings, Src emerges as a critical upstream regulator of both PKC-iota and the NF-kappaB pathway.

Indexed as

Signal TransductionAmino Acid SequenceAnimalsCell DifferentiationCell SurvivalEnzyme ActivationI-kappa B KinaseIsoenzymesJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesMolecular Sequence DataNerve Growth FactorNF-kappa Bp38 Mitogen-Activated Protein KinasesPC12 CellsI-kappa B KinaseIsoenzymesJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesNerve Growth FactorNF-kappa Bp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPKC-3 proteinProtein Kinase CProtein Kinase C-lambdaProtein Serine-Threonine KinasesProto-Oncogene Proteins c-rafras Proteinssrc-Family Kinases

Identifiers

PMID10848576
PMCPMC85825
OpenAlexW2122210284

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.