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Article

Evidence against GRB10 as the gene responsible for Silver-Russell syndrome.

Biochemical and biophysical research communications - 7 Sept 2001

McCann J A, Zheng H, Islam A, Goodyer C G, Polychronakos C

Abstract excerpt

Recent evidence shows that Silver-Russell syndrome (SRS), the major functional deficit of which is limited growth, both intrauterine and postnatal, is due to a double dose of a gene within 7p11.2-p13 that is normally expressed exclusively from the maternal copy. Of the several growth-related genes in this chromosomal region, only GRB10 has been demonstrated to be imprinted; however, imprinting was limited to...

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Source

Identifiers

PMID: 11527390
DOI: 10.1006/bbrc.2001.5500

Genes

GRB10

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Evidence against GRB10 as the gene responsible for Silver-Russell syndrome.PMID 11527390Read ↗

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Imprinting of human GRB10 and its mutations in two patients with Russell-Silver syndrome.Semantic proximity Read ↗

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Heterogeneous growth patterns in carriers of chromosome 7p12.2 imbalances affecting GRB10.Semantic proximity Read ↗

PEG10 loss of function causes Silver-Russell syndrome: a familial case with paternal deletion.Semantic proximity Read ↗

Phenotype of genetically confirmed Silver-Russell syndrome beyond childhood.Semantic proximity Read ↗

Silver-Russell syndrome: a dissection of the genetic aetiology and candidate chromosomal regions.Semantic proximity Read ↗

Conserved methylation imprints in the human and mouse GRB10 genes with divergent allelic expression suggests differential reading of the same markSemantic proximity Read ↗

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DDC and COBL, flanking the imprinted GRB10 gene on 7p12, are biallelically expressed.Semantic proximity Read ↗

Human GRB10 is imprinted and expressed from the paternal and maternal allele in a highly tissue- and isoform-specific fashion.Semantic proximity Read ↗

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