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Article

Multiple Sp1 sites efficiently drive transcription of the TATA-less promoter of the human glypican 3 (GPC3) gene.

Gene - 3 Jul 1998

Huber R, Schlessinger D, Pilia G

Abstract excerpt

Simpson-Golabi-Behmel Syndrome (SGBS) is an X-linked disease characterized by pre- and postnatal overgrowth. Recently, we have shown that mutations in the glypican family gene, GPC3, cause SGBS. This gene is predominantly expressed in the same mesoderm-derived tissues that overgrow in its absence. To investigate the basis for promoter function, 3.3kb of GC-rich DNA 5' of the transcribed region were fused to a...

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Source

Identifiers

PMID: 9651473
DOI: 10.1016/s0378-1119(98)00233-9

Genes

GPC3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Multiple Sp1 sites efficiently drive transcription of the TATA-less promoter of the human glypican 3 (GPC3) gene.PMID 9651473Read ↗

Characterization of the 5′-regulatory region of the human thiamin transporter <i>SLC19A3</i>: in vitro and in vivo studiesSemantic proximity Read ↗

GPC3 mutation analysis in a spectrum of patients with overgrowth expands the phenotype of Simpson-Golabi-Behmel syndrome.Semantic proximity Read ↗

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Gene expression of the human glucagon-like peptide-1 receptor is regulated by Sp1 and Sp3.Semantic proximity Read ↗

Molecular analysis of a novel intragenic deletion in GPC3 in three cousins with Simpson-Golabi-Behmel syndrome.Semantic proximity Read ↗

Mutational analysis of the GPC3/GPC4 glypican gene cluster on Xq26 in patients with Simpson-Golabi-Behmel syndrome: identification of loss-of-function mutations in the GPC3 gene.Semantic proximity Read ↗

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Sp3 represses gene expression via the titration of promoter-specific transcription factors.Semantic proximity Read ↗

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