Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The critical role of Shc in insulin-like growth factor-I-mediated mitogenesis and differentiation in 3T3-L1 preadipocytes.

Molecular endocrinology (Baltimore, Md.) - 1 Jun 2000

Boney C M, Gruppuso P A, Faris R A, Frackelton A R

Abstract excerpt

Insulin-like growth factor-I (IGF-I) stimulates mitogenesis in proliferating preadipocytes, but when cells reach confluence and become growth arrested, IGF-I stimulates differentiation into adipocytes. IGF-I induces signaling pathways that involve IGF-I receptor-mediated tyrosine phosphorylation of Shc and insulin receptor substrate 1 (IRS-1). Either of these adaptor proteins can lead to activation of the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to 3T3 Cells
Share to Adaptor Proteins, Vesicular Transport

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Adipocytes

Share to Flavonoids

Share to Insulin-Like Growth Factor I

Share to Mitogen-Activated Protein Kinases

Share to Shc Signaling Adaptor Proteins

Share to Src Homology 2 Domain-Containing, Transforming Protein 1

Source

Identifiers

PMID: 10847583
DOI: 10.1210/mend.14.6.0487

Genes

LPL

Variants

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

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The critical role of Shc in insulin-like growth factor-I-mediated mitogenesis and differentiation in 3T3-L1 preadipocytes.PMID 10847583Read ↗

Tyrosine phosphorylation-dependent and -independent role of Shc in the regulation of IGF-1-induced mitogenesis and glycogen synthesis.Semantic proximity Read ↗

FMIP controls the adipocyte lineage commitment of C2C12 cells by downmodulation of C/EBP alpha.Semantic proximity Read ↗

Clk/STY (cdc2-like kinase 1) and Akt regulate alternative splicing and adipogenesis in 3T3-L1 pre-adipocytes.Semantic proximity Read ↗

Role of SHPS-1 in the regulation of insulin-like growth factor I-stimulated Shc and mitogen-activated protein kinase activation in vascular smooth muscle cells.Semantic proximity Read ↗

Mechanism of SHIP-mediated inhibition of insulin- and platelet-derived growth factor-stimulated mitogen-activated protein kinase activity in 3T3-L1 adipocytes.Semantic proximity Read ↗

Extracellular signal-regulated kinase-1 and -2 respond differently to mitogenic and differentiative signaling pathways in myoblasts.Semantic proximity Read ↗

Differential Roles of Insulin Receptor Substrates in Brown Adipocyte DifferentiationSemantic proximity Read ↗

Insulin-like growth factor-I-stimulated insulin receptor substrate-1 negatively regulates Src homology 2 domain-containing protein-tyrosine phosphatase substrate-1 function in vascular smooth muscle cells.Semantic proximity Read ↗

Roles of insulin receptor substrate-1 and Shc on insulin-like growth factor I receptor signaling in early passages of cultured human fibroblasts.Semantic proximity Read ↗

Insulin receptor substrate-1/SHP-2 interaction, a phenotype-dependent switching machinery of insulin-like growth factor-I signaling in vascular smooth muscle cells.Semantic proximity Read ↗

Requirement for PIKfyve enzymatic activity in acute and long-term insulin cellular effects.Semantic proximity Read ↗

Protein kinase C-delta is an important signaling molecule in insulin-like growth factor I receptor-mediated cell transformation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.