PMID- 10500192
OWN - NLM
STAT- MEDLINE
DCOM- 19991021
LR  - 20190501
IS  - 0027-8424 (Print)
IS  - 0027-8424 (Linking)
VI  - 96
IP  - 20
DP  - 1999 Sep 28
TI  - Genomic sequence, structural organization, molecular evolution, and aberrant
      rearrangement of promyelocytic leukemia zinc finger gene.
PG  - 11422-7
AB  - The promyelocytic leukemia zinc finger gene (PLZF) is involved in chromosomal
      translocation t(11;17) associated with acute promyelocytic leukemia. In this
      work, a 201-kilobase genomic DNA region containing the entire PLZF gene was
      sequenced. Repeated elements account for 19.83%, and no obvious coding
      information other than PLZF is present over this region. PLZF contains six exons 
      and five introns, and the exon organization corresponds well with protein
      domains. There are at least four alternative splicings (AS-I, -II, -III, and -IV)
      within exon 1. AS-I could be detected in most tissues tested whereas AS-II, -III,
      and -IV were present in the stomach, testis, and heart, respectively. Although
      splicing donor and acceptor signals at exon-intron boundaries for AS-I and exons 
      1-6 were classical (gt-ag), AS-II, -III, and -IV had atypical splicing sites.
      These alternative splicings, nevertheless, maintained the ORF and may encode
      isoforms with absence of important functional domains. In mRNA species without
      AS-I, there is a relatively long 5' UTR of 6.0 kilobases. A TATA box and several 
      transcription factor binding sites were found in the putative promoter region
      upstream of the transcription start site. PLZF is a well conserved gene from
      Caenorhabditis elegans to human. PLZF paralogous sequences are found in human
      genome. The presence of two MLL/PLZF-like alignments on human chromosome 11q23
      and 19 suggests a syntenic replication during evolution. The chromosomal
      breakpoints and joining sites in the index acute promyelocytic leukemia case with
      t(11;17) also were characterized, which suggests the involvement of DNA
      damage-repair mechanism.
FAU - Zhang, T
AU  - Zhang T
AD  - Key Laboratory of Human Genome Research, Ministry of Public Health, Ruijin
      Hospital, Shanghai 200025, USA.
FAU - Xiong, H
AU  - Xiong H
FAU - Kan, L X
AU  - Kan LX
FAU - Zhang, C K
AU  - Zhang CK
FAU - Jiao, X F
AU  - Jiao XF
FAU - Fu, G
AU  - Fu G
FAU - Zhang, Q H
AU  - Zhang QH
FAU - Lu, L
AU  - Lu L
FAU - Tong, J H
AU  - Tong JH
FAU - Gu, B W
AU  - Gu BW
FAU - Yu, M
AU  - Yu M
FAU - Liu, J X
AU  - Liu JX
FAU - Licht, J
AU  - Licht J
FAU - Waxman, S
AU  - Waxman S
FAU - Zelent, A
AU  - Zelent A
FAU - Chen, E
AU  - Chen E
FAU - Chen, S J
AU  - Chen SJ
LA  - eng
SI  - GENBANK/AF060568
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (Promyelocytic Leukemia Zinc Finger Protein)
RN  - 0 (RARA protein, human)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoic Acid Receptor alpha)
RN  - 0 (Transcription Factors)
RN  - 147855-37-6 (ZBTB16 protein, human)
SB  - IM
MH  - Alternative Splicing
MH  - Base Sequence
MH  - DNA-Binding Proteins/*genetics
MH  - Exons
MH  - *Gene Rearrangement
MH  - Genes, Regulator
MH  - Humans
MH  - Introns
MH  - Kruppel-Like Transcription Factors
MH  - Molecular Sequence Data
MH  - Promyelocytic Leukemia Zinc Finger Protein
MH  - Receptors, Retinoic Acid/genetics
MH  - Recombination, Genetic
MH  - Retinoic Acid Receptor alpha
MH  - TATA Box
MH  - Transcription Factors/*genetics
MH  - Zinc Fingers/*genetics
PMC - PMC18049
EDAT- 1999/09/29 00:00
MHDA- 1999/09/29 00:01
CRDT- 1999/09/29 00:00
PHST- 1999/09/29 00:00 [pubmed]
PHST- 1999/09/29 00:01 [medline]
PHST- 1999/09/29 00:00 [entrez]
AID - 10.1073/pnas.96.20.11422 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11422-7. doi:
      10.1073/pnas.96.20.11422.