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

Selective coupling of STAT factors to the mouse prolactin receptor.

European journal of biochemistry - 1 Dec 1998

Mayr S, Welte T, Windegger M, Lechner J, May P, Heinrich P C, Horn F, Doppler W

Abstract excerpt

Prolactin has been reported to induce distinct sets of signal transducers and activators of transcription (STAT) in a cell-type-specific fashion. In the mammary epithelium, although STAT1, STAT3, STAT5A, STAT5B and STAT6 are present in a latent form, only STAT5A and STAT5B are activated. This selective activation of STAT5 by prolactin was also observed in COS-7 cells cotransfected with the long form of the mouse...

Read the complete abstract on PubMed

Topics

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

Share to Binding Sites
Share to Cell Line
Share to DNA-Binding Proteins

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

Share to Mutation

Share to Promoter Regions, Genetic

Share to Recombinant Fusion Proteins

Share to Sequence Alignment

Source

Identifiers

PMID: 9874248
DOI: 10.1046/j.1432-1327.1998.2580784.x

Genes

PRL
STAT1
STAT3
STAT6
EPO

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

Selective coupling of STAT factors to the mouse prolactin receptor.PMID 9874248Read ↗

Expression of a carboxy terminally truncated Stat5 with no transactivation domain in the mammary glands of transgenic mice inhibits cell proliferation during pregnancy, delays onset of milk secretion, and induces apoptosis upon involution.Semantic proximity Read ↗

Deletion of the carboxyl-terminal transactivation domain of MGF-Stat5 results in sustained DNA binding and a dominant negative phenotype.Semantic proximity Read ↗

Naturally occurring dominant negative variants of Stat5.Semantic proximity Read ↗

A Sequence of the CIS Gene Promoter Interacts Preferentially with Two Associated STAT5A Dimers: a Distinct Biochemical Difference between STAT5A and STAT5BSemantic proximity Read ↗

STAT5B SH2 variants disrupt mammary enhancers and the stability of genetic programs during pregnancySemantic proximity Read ↗

Role of Prolactin/Prolactin Receptor Signaling in Human Breast CancerSemantic proximity Read ↗

Experimental regulation of STAT gene expression reveals an involvement of STAT5 in interleukin-4-driven cell proliferation.Semantic proximity Read ↗

The coactivator of transcription CREB-binding protein interacts preferentially with the glycosylated form of Stat5.Semantic proximity Read ↗

Overexpression and forced activation of stat5 in mammary gland of transgenic mice promotes cellular proliferation, enhances differentiation, and delays postlactational apoptosis.Semantic proximity Read ↗

Unexpected functional role of the transactivation domain for nuclear import of STAT5Semantic proximity Read ↗

Regulation of erythropoietin-induced STAT serine phosphorylation by distinct mitogen-activated protein kinases.Semantic proximity Read ↗

Threonine 391 phosphorylation of the human prolactin receptor mediates a novel interaction with 14-3-3 proteins.Semantic proximity Read ↗

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