PMID- 10072440
OWN - NLM
STAT- MEDLINE
DCOM- 19990429
LR  - 20190513
IS  - 0964-6906 (Print)
IS  - 0964-6906 (Linking)
VI  - 8
IP  - 4
DP  - 1999 Apr
TI  - Isolation and embryonic expression of the novel mouse gene Hic1, the homologue of
      HIC1, a candidate gene for the Miller-Dieker syndrome.
PG  - 697-710
AB  - The human gene HIC1 (hypermethylated in cancer) maps to chromosome 17p13.3 and is
      deleted in the contiguous gene disorder Miller-Dieker syndrome (MDS) [Makos-Wales
      et al. (1995) Nature Med., 1, 570-577; Chong et al. (1996) Genome Res., 6,
      735-741]. We isolated the murine homologue Hic1, encoding a zinc-finger protein
      with a poxvirus and zinc-finger (POZ) domain and mapped it to mouse chromosome 11
      in a region exhibiting conserved synteny to human chromosome 17. Comparison of
      genomic and cDNA sequences predicts two exons for the murine Hic1. The second
      exon exhibits 88% identity to the human HIC1 on DNA level. During embryonic
      development, Hic1 is expressed in mesenchymes of the sclerotomes, lateral body
      wall, limb and cranio-facial regions embedding the outgrowing peripheral nerves
      during their differentiation. During fetal development, Hic1 additionally is
      expressed in mesenchymes apposed to precartilaginous condensations, at many
      interfaces to budding epithelia of inner organs, and weakly in muscles. We
      observed activation of Hic1 expression in the embryonic anlagen of many tissues
      displaying anomalies in MDS patients. Besides lissencephaly, MDS patients exhibit
      facial dysmorphism and frequently additional birth defects, e.g. anomalies of the
      heart, kidney, gastrointestinal tract and the limbs (OMIM 247200). Thus, HIC1
      activity may correlate with the defective development of the nose, jaws,
      extremities, gastrointestinal tract and kidney in MDS patients.
FAU - Grimm, C
AU  - Grimm C
AD  - GSF-National Research Center for Environment and Health, Institute of Mammalian
      Genetics, D-85764 Neuherberg, Germany.
FAU - Sporle, R
AU  - Sporle R
FAU - Schmid, T E
AU  - Schmid TE
FAU - Adler, I D
AU  - Adler ID
FAU - Adamski, J
AU  - Adamski J
FAU - Schughart, K
AU  - Schughart K
FAU - Graw, J
AU  - Graw J
LA  - eng
SI  - GENBANK/AF036334
SI  - GENBANK/AF036582
SI  - GENBANK/AF111712
PT  - Journal Article
PL  - England
TA  - Hum Mol Genet
JT  - Human molecular genetics
JID - 9208958
RN  - 0 (Hic1 protein, mouse)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factors)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Abnormalities, Multiple/*genetics
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Brain/*abnormalities
MH  - Chromosome Mapping
MH  - DNA/chemistry/genetics/isolation & purification
MH  - Embryo, Mammalian/chemistry
MH  - Fetus/chemistry
MH  - Gene Expression Regulation, Developmental
MH  - Genes, Tumor Suppressor/*genetics
MH  - In Situ Hybridization
MH  - In Situ Hybridization, Fluorescence
MH  - Kruppel-Like Transcription Factors
MH  - Mesoderm/chemistry
MH  - Mice
MH  - Mice, Inbred C3H
MH  - Mice, Inbred C57BL
MH  - Molecular Sequence Data
MH  - RNA, Messenger/genetics/metabolism
MH  - Sequence Alignment
MH  - Sequence Analysis, DNA
MH  - Sequence Homology, Amino Acid
MH  - Syndrome
MH  - Tissue Distribution
MH  - Transcription Factors/*genetics
EDAT- 1999/03/11 00:00
MHDA- 1999/03/11 00:01
CRDT- 1999/03/11 00:00
PHST- 1999/03/11 00:00 [pubmed]
PHST- 1999/03/11 00:01 [medline]
PHST- 1999/03/11 00:00 [entrez]
AID - ddc082 [pii]
AID - 10.1093/hmg/8.4.697 [doi]
PST - ppublish
SO  - Hum Mol Genet. 1999 Apr;8(4):697-710. doi: 10.1093/hmg/8.4.697.