PMID- 10409750
OWN - NLM
STAT- MEDLINE
DCOM- 19990819
LR  - 20190508
IS  - 0270-7306 (Print)
IS  - 0270-7306 (Linking)
VI  - 19
IP  - 8
DP  - 1999 Aug
TI  - Pro-B-cell-specific transcription and proapoptotic function of protein kinase
      Ceta.
PG  - 5608-18
AB  - Using a subtractive cloning scheme on cDNA prepared from primary pro-B and pre-B 
      cells, we identified several genes whose products regulate apoptosis. We further 
      characterized one of these genes, encoding protein kinase Ceta (PKCeta). PKCeta
      transcripts were readily detected in pro-B cells but were absent in pre-B cells. 
      Although both a full-length and a truncated form of PKCeta were detectable in
      bone marrow pro-B cells, transition to the pre-B-cell stage was associated with
      increased relative levels of truncated PKCeta. We found that PKCeta is
      proteolyzed in apoptotic lymphocytes, generating a kinase-active fragment
      identical to the truncated form which is capable of inducing apoptosis when
      expressed in a pro-B cell line. Caspase-3 can generate an identical PKCeta
      cleavage product in vitro, and caspase inhibitors prevent the generation of this 
      product during apoptosis in transfected cell lines. Inducible overexpression of
      either the full-length or truncated form of PKCeta results in cell cycle arrest
      at the G(1)/S transition. These results suggest that the expression and
      proteolytic activation of PKCeta play an important role in the regulation of cell
      division and cell death during early B-cell development.
FAU - Morrow, T A
AU  - Morrow TA
AD  - Graduate Program in Immunology, The Johns Hopkins University School of Public
      Health, Baltimore, Maryland 21205, USA.
FAU - Muljo, S A
AU  - Muljo SA
FAU - Zhang, J
AU  - Zhang J
FAU - Hardwick, J M
AU  - Hardwick JM
FAU - Schlissel, M S
AU  - Schlissel MS
LA  - eng
GR  - R01 HL48702/HL/NHLBI NIH HHS/United States
GR  - R01 NS034175/NS/NINDS NIH HHS/United States
GR  - R01 HL048702/HL/NHLBI NIH HHS/United States
GR  - R01 NS34175/NS/NINDS NIH HHS/United States
GR  - T32 AI07247/AI/NIAID NIH HHS/United States
GR  - T32 AI007247/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (DNA, Complementary)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (Isoenzymes)
RN  - 0 (Peptide Fragments)
RN  - 0 (RNA, Messenger)
RN  - 0 (Serine Proteinase Inhibitors)
RN  - 128559-51-3 (RAG-1 protein)
RN  - EC 2.7.1.- (protein kinase C eta)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 3.4.22.- (Casp3 protein, mouse)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Animals
MH  - Apoptosis/*genetics
MH  - B-Lymphocytes/*cytology/enzymology
MH  - Caspase 3
MH  - Caspases/physiology
MH  - Cell Cycle
MH  - Cell Lineage
MH  - DNA, Complementary/genetics
MH  - Enzyme Induction
MH  - *Gene Expression Regulation, Developmental
MH  - Hematopoiesis/*genetics
MH  - Hematopoietic Stem Cells/*cytology/enzymology
MH  - Homeodomain Proteins/genetics/physiology
MH  - Isoenzymes/genetics/*physiology
MH  - Mice
MH  - Mice, Knockout
MH  - Organ Specificity
MH  - Peptide Fragments/metabolism
MH  - Protein Kinase C/genetics/*physiology
MH  - Protein Processing, Post-Translational
MH  - RNA, Messenger/biosynthesis
MH  - Serine Proteinase Inhibitors/pharmacology
MH  - Subtraction Technique
MH  - *Transcription, Genetic
MH  - Transfection
PMC - PMC84413
EDAT- 1999/07/20 00:00
MHDA- 1999/07/20 00:01
CRDT- 1999/07/20 00:00
PHST- 1999/07/20 00:00 [pubmed]
PHST- 1999/07/20 00:01 [medline]
PHST- 1999/07/20 00:00 [entrez]
AID - 10.1128/mcb.19.8.5608 [doi]
PST - ppublish
SO  - Mol Cell Biol. 1999 Aug;19(8):5608-18. doi: 10.1128/mcb.19.8.5608.