ArticleThe Journal of clinical investigation1998
Biological effects of targeted inactivation of hepatocyte growth factor-like protein in mice.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 75 citations in OpenAlex.
- MSP-RON signaling in liver pathobiology and as an emerging therapeutic target: a review of the current evidence.Cell communication and signaling : CCS · 2025Review
- Review
- Gut microbiota and blood biomarkers in IBD-Related arthritis: insights from mendelian randomization.Scientific reports · 2025Article
- Central subfield thickness of diabetic macular edema: Correlation with the aqueous humor proteome.Molecular vision · 2024Article
- Macrophage-Stimulating Protein Enhances Osteoblastic Differentiation via the Recepteur d'Origine Nantais Receptor and Extracellular Signal-Regulated Kinase Signaling Pathway.Journal of bone metabolism · 2020Article
- Regulation of Energy Metabolism by Receptor Tyrosine Kinase Ligands.Frontiers in physiology · 2020Review
- HGFL-mediated RON signaling supports breast cancer stem cell phenotypes via activation of non-canonical β-catenin signaling.Oncotarget · 2017Article
- MSP is a negative regulator of inflammation and lipogenesis in ex vivo models of non-alcoholic steatohepatitis.Experimental & molecular medicine · 2016Article
- HGFL supports mammary tumorigenesis by enhancing tumor cell intrinsic survival and influencing macrophage and T-cell responses.Oncotarget · 2015Article
- Novel serum biomarkers for detection of excessive alcohol use.Alcoholism, clinical and experimental research · 2015Article
- Expression of Hepatocyte Growth Factor-Like Protein in Human Wound Tissue and Its Biological Functionality in Human Keratinocytes.Biomedicines · 2015Article
- Hepatocyte growth factor-like protein is a positive regulator of early mammary gland ductal morphogenesis.Mechanisms of development · 2014Article
- Hepatocyte growth factor-like protein is required for prostate tumor growth in the TRAMP mouse model.Oncotarget · 2014Article
- MSP-RON signalling in cancer: pathogenesis and therapeutic potential.Nature reviews. Cancer · 2013Review
- Macrophage-stimulating protein and calcium homeostasis in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Article
- The Ron receptor tyrosine kinase positively regulates angiogenic chemokine production in prostate cancer cells.Oncogene · 2010Article
- The RON receptor tyrosine kinase promotes MSP-independent cell spreading and survival in breast epithelial cells.Oncogene · 2009Article
- Ron receptor tyrosine kinase-dependent hepatic neutrophil recruitment and survival benefit in a murine model of bacterial peritonitis.Critical care medicine · 2008Article
- Met-related receptor tyrosine kinase Ron in tumor growth and metastasis.Advances in cancer research · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hepatocyte growth factor-like protein (HGFL) is a liver-derived serum glycoprotein involved in cell proliferation and differentiation, and is proposed to have a fundamental role in embryogenesis, fertility, hematopoiesis, macrophage activation, and tissue repair. To assess the in vivo effects of total loss of HGFL, we generated mice with targeted disruption of the gene resulting in loss of the protein. Disruption of the HGFL gene allowed for normal embryogenesis, and followed a Mendelian pattern of genetic transmission. Mice homozygous for the targeted allele (HGFL-/- mice) are fertile, and grow to adulthood without obvious phenotypic abnormalities in unchallenged animals, except for development of lipid-containing cytoplasmic vacuoles in hepatocytes throughout the liver lobules. These histologic changes are not accompanied by discernible changes in synthetic or excretory hepatic functions. Hematopoiesis appears unaltered, and although macrophage activation is delayed in the absence of HGFL, migration to the peritoneal cavity upon challenge with thioglycollate was similar in HGFL-/- and wild-type mice. Challenged with incision to skin, HGFL-/- mice display normal wound healing. These data demonstrate that HGFL is not essential for embryogenesis, fertility, or wound healing. HGFL-deficient mice will provide a valuable means to assess the role of HGFL in hepatic and systemic responses to inflammatory and infectious stimuli in vivo.
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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.