PMID- 10644770
OWN - NLM
STAT- MEDLINE
DCOM- 20000229
LR  - 20190508
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 275
IP  - 4
DP  - 2000 Jan 28
TI  - ESE-3, a novel member of an epithelium-specific ets transcription factor
      subfamily, demonstrates different target gene specificity from ESE-1.
PG  - 2986-98
AB  - Most cancers originate as a result of aberrant gene expression in mainly
      glandular epithelial tissues leading to defects in epithelial cell
      differentiation. The latter is governed by distinct sets of transcriptional
      regulators. Here we report the characterization of epithelium-specific Ets
      factor, family member 3 (ESE-3), a novel member of the ESE subfamily of Ets
      transcription factors. ESE-3 shows highest homology to two other epithelium
      restricted Ets factors, ESE-1 and ESE-2. ESE-3, like ESE-1 and ESE-2, is
      exclusively expressed in a subset of epithelial cells with highest expression in 
      glandular epithelium such as prostate, pancreas, salivary gland, and trachea. A
      potential role in branching morphogenesis is suggested, since ESE-3
      transactivates the c-MET promoter via three high affinity binding sites.
      Additionally, ESE-3 binding to DNA sequences in the promoters of several
      glandular epithelium-specific genes suggests a role for ESE-3 in later stages of 
      glandular epithelium differentiation. Although ESE-3 and ESE-1 bind with similar 
      affinity to various Ets binding sites, ESE-3 and ESE-1 differ significantly in
      their ability to transactivate the promoters containing these sites. Our results 
      support the notion that ESE-1, ESE-2, and ESE-3 represent a unique
      epithelium-specific subfamily of Ets factors that have critical but distinct
      functions in epithelial cell differentiation and proliferation.
FAU - Kas, K
AU  - Kas K
AD  - New England Baptist Bone and Joint Institute, Beth Israel Deaconess Medical
      Center, and Harvard Medical School, Boston, Massachusetts 02115, USA.
FAU - Finger, E
AU  - Finger E
FAU - Grall, F
AU  - Grall F
FAU - Gu, X
AU  - Gu X
FAU - Akbarali, Y
AU  - Akbarali Y
FAU - Boltax, J
AU  - Boltax J
FAU - Weiss, A
AU  - Weiss A
FAU - Oettgen, P
AU  - Oettgen P
FAU - Kapeller, R
AU  - Kapeller R
FAU - Libermann, T A
AU  - Libermann TA
LA  - eng
SI  - GENBANK/AF124438
SI  - GENBANK/AF124439
GR  - KO8/CA 71429/CA/NCI NIH HHS/United States
GR  - R01 CA76323/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  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Adaptor Proteins, Vesicular Transport)
RN  - 0 (Carrier Proteins)
RN  - 0 (DNA, Complementary)
RN  - 0 (EHF protein, human)
RN  - 0 (ITSN1 protein, human)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-ets)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - *Adaptor Proteins, Vesicular Transport
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Carrier Proteins/*metabolism
MH  - Cells, Cultured
MH  - Cloning, Molecular
MH  - DNA, Complementary
MH  - Epithelium/metabolism
MH  - *Gene Targeting
MH  - Humans
MH  - Molecular Sequence Data
MH  - Multigene Family
MH  - Phylogeny
MH  - Promoter Regions, Genetic
MH  - Proto-Oncogene Proteins/*genetics/metabolism
MH  - Proto-Oncogene Proteins c-ets
MH  - Sequence Homology, Amino Acid
MH  - Transcription Factors/*genetics/metabolism
MH  - Transcriptional Activation
EDAT- 2000/01/25 09:00
MHDA- 2000/03/04 09:00
CRDT- 2000/01/25 09:00
PHST- 2000/01/25 09:00 [pubmed]
PHST- 2000/03/04 09:00 [medline]
PHST- 2000/01/25 09:00 [entrez]
AID - 10.1074/jbc.275.4.2986 [doi]
PST - ppublish
SO  - J Biol Chem. 2000 Jan 28;275(4):2986-98. doi: 10.1074/jbc.275.4.2986.