PMID- 9488476
OWN - NLM
STAT- MEDLINE
DCOM- 19980319
LR  - 20240409
IS  - 0270-7306 (Print)
IS  - 1098-5549 (Electronic)
IS  - 0270-7306 (Linking)
VI  - 18
IP  - 3
DP  - 1998 Mar
TI  - Gene expression and cell cycle arrest mediated by transcription factor DMP1 is 
      antagonized by D-type cyclins through a cyclin-dependent-kinase-independent 
      mechanism.
PG  - 1590-600
AB  - A novel 761-amino-acid transcription factor, DMP1, contains a central DNA binding 
      domain that includes three imperfect myb repeats flanked by acidic 
      transactivating domains at the amino and carboxyl termini. D-type cyclins 
      associate with a region of the DMP1 DNA binding domain immediately adjacent to 
      the myb repeats to form heteromeric complexes which detectably interact neither 
      with cyclin-dependent kinase 4 (CDK4) nor with DNA. The segment of D-type cyclins 
      required for its interaction with DMP1 falls outside the "cyclin box," which 
      contains the residues predicted to contact CDK4. Hence, D-type cyclin point 
      mutants that do not interact with CDK4 can still bind to DMP1. Enforced 
      coexpression of either of three D-type cyclins (D1, D2, or D3) with DMP1 in 
      mammalian cells canceled its ability to activate gene expression. This property 
      was not shared by cyclins A, B, C, or H; did not depend upon CDK4 or CDK2 
      coexpression; was not subverted by a mutation in cyclin D1 that prevents its 
      interaction with CDK4; and was unaffected by inhibitors of CDK4 catalytic 
      activity. Introduction of DMP1 into mouse NIH 3T3 fibroblasts inhibited entry 
      into S phase. Cell cycle arrest depended upon the ability of DMP1 to bind to DNA 
      and to transactivate gene expression and was specifically antagonized by 
      coexpression of D-type cyclins, including a D1 point mutant that does not bind to 
      CDK4. Taken together, these findings suggest that DMP1 induces genes that inhibit 
      S phase entry and that D-type cyclins can override DMP1-mediated growth arrest in 
      a CDK-independent manner.
FAU - Inoue, K
AU  - Inoue K
AD  - Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, 
      Tennessee 38105, USA.
FAU - Sherr, C J
AU  - Sherr CJ
LA  - eng
GR  - P30 CA021765/CA/NCI NIH HHS/United States
GR  - CA-20180/CA/NCI NIH HHS/United States
GR  - CA21765/CA/NCI 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 (DMTF1 protein, human)
RN  - 0 (Dmtf1 protein, mouse)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Transcription Factors)
RN  - 136601-57-5 (Cyclin D1)
RN  - 9007-49-2 (DNA)
RN  - EC 2.7.11.22 (CDK4 protein, human)
RN  - EC 2.7.11.22 (Cdk4 protein, mouse)
RN  - EC 2.7.11.22 (Cyclin-Dependent Kinase 4)
RN  - EC 2.7.11.22 (Cyclin-Dependent Kinases)
SB  - IM
MH  - 3T3 Cells
MH  - Animals
MH  - Binding Sites
MH  - *Cell Cycle
MH  - Cell Division
MH  - Cell Line
MH  - Chromosome Mapping
MH  - Cyclin D1/genetics/*metabolism
MH  - Cyclin-Dependent Kinase 4
MH  - Cyclin-Dependent Kinases/genetics/*metabolism
MH  - DNA/metabolism
MH  - Gene Expression
MH  - Humans
MH  - Mice
MH  - *Proto-Oncogene Proteins
MH  - Recombinant Fusion Proteins/genetics/metabolism
MH  - Spodoptera/cytology
MH  - Transcription Factors/antagonists & inhibitors/genetics/*metabolism
MH  - Transcriptional Activation
PMC - PMC108874
EDAT- 1998/03/06 00:00
MHDA- 1998/03/06 00:01
PMCR- 1998/03/01
CRDT- 1998/03/06 00:00
PHST- 1998/03/06 00:00 [pubmed]
PHST- 1998/03/06 00:01 [medline]
PHST- 1998/03/06 00:00 [entrez]
PHST- 1998/03/01 00:00 [pmc-release]
AID - 1305 [pii]
AID - 10.1128/MCB.18.3.1590 [doi]
PST - ppublish
SO  - Mol Cell Biol. 1998 Mar;18(3):1590-600. doi: 10.1128/MCB.18.3.1590.