ArticleMolecular endocrinology (Baltimore, Md.)2008
JAK2, but not Src family kinases, is required for STAT, ERK, and Akt signaling in response to growth hormone in preadipocytes and hepatoma cells.
Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed.
- Identification of βIIΣ1-Spectrin as a Binding Partner of the GH-regulated Human Obesity Scaffold Protein SH2B1.Endocrinology · 2025Article
- Exploring the therapeutic potential andFrontiers in pharmacology · 2025Article
- Review
- Identification of a novelMolecular medicine reports · 2022Article
- Article
- Blockade of growth hormone receptor signaling by using pegvisomant: A functional therapeutic strategy in hepatocellular carcinoma.Frontiers in oncology · 2022Article
- Classical and novel GH receptor signaling pathways.Molecular and cellular endocrinology · 2020Review
- Glucose-Regulated Protein 94 (GRP94): A Novel Regulator of Insulin-Like Growth Factor Production.Cells · 2020Review
- Growth Hormone Receptor Regulation in Cancer and Chronic Diseases.Frontiers in endocrinology · 2020Review
- Activation of STAT1 by the FRK tyrosine kinase is associated with human glioma growth.Journal of neuro-oncology · 2019Article
- Nonclassical GH Insensitivity: Characterization of Mild Abnormalities of GH Action.Endocrine reviews · 2019Review
- Renal expression of JAK2 is high in polycystic kidney disease and its inhibition reduces cystogenesis.Scientific reports · 2019Article
- Growth Hormone and Insulin-Like Growth Factor Action in Reproductive Tissues.Frontiers in endocrinology · 2019Review
- The effects of growth hormone on therapy resistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2019Article
- Article
- MERTK signaling in the retinal pigment epithelium regulates the tyrosine phosphorylation of GDP dissociation inhibitor alpha from the GDI/CHM family of RAB GTPase effectors.Experimental eye research · 2015Article
- JAK2 activation by growth hormone and other cytokines.The Biochemical journal · 2015Review
- Minireview: mechanisms of growth hormone-mediated gene regulation.Molecular endocrinology (Baltimore, Md.) · 2014Review
- Dysregulated STAT1-SOCS1 control of JAK2 promotes mammary luminal progenitor cell survival and drives ERα(+) tumorigenesis.Cell death and differentiation · 2014Article
- Growth hormone and insulin-like growth factor-I alter hippocampal excitatory synaptic transmission in young and old rats.Age (Dordrecht, Netherlands) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Janus kinase 2 (JAK2), a tyrosine kinase that associates with the GH receptor and is activated by GH, has been implicated as a key mediator of GH signaling. Several published reports suggest that members of the Src family of tyrosine kinases may also participate in GH signaling. We therefore investigated the extent to which JAK2 and Src family kinases mediate GH activation of signal transducers and activators of transcription (STATs) 1, 3, and 5a/b, ERKs 1 and 2, and Akt, in the highly GH-responsive cell lines 3T3-F442A preadipocytes and H4IIE hepatoma cells. GH activation of Src family kinases was not detected in either cell line. Further, blocking basal activity of Src kinases with the Src inhibitors PP1 and PP2 did not inhibit GH activation of STATs 1, 3, or 5a/b, or ERKs 1 and 2. When levels of JAK2 were depressed by short hairpin RNA in 3T3-F442A and H4IIE cells, GH-stimulated activation of STATs 1, 3, and 5a/b, ERKs 1 and 2, and Akt were significantly reduced; however, basal activity of Src family kinases was unaffected. These results were supported genetically by experiments showing that GH robustly activates JAK2, STATs 3 and 5a/b, ERKs 1 and 2, and Akt in murine embryonic fibroblasts derived from Src/Yes/ Fyn triple-knockout embryos that lack known Src kinases. These results strongly suggest that JAK2, but not Src family kinases, is critical for transducing these GH signals in 3T3-F442A and H4IIE cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.