Evidence map›Paper›PMID 11832492›Full record

ArticleThe Journal of biological chemistry2002

Differential mitogenic effects of single chain hepatocyte growth factor (HGF)/scatter factor and HGF/NK1 following cleavage by factor Xa.

Peter Pediaditakis, Satdarshan P S Monga, Wendy M Mars, George K Michalopoulos

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 32% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. MET: a critical player in tumorigenesis and therapeutic target.Cold Spring Harbor perspectives in biology · 2013
    Review
  5. Article
  6. Article
  7. A mechanistic basis for converting a receptor tyrosine kinase agonist to an antagonist.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  8. Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Peter PediaditakisDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261.
Satdarshan P S Monga
Wendy M Mars
George K Michalopoulos
University of Pittsburgh · US

Funding

HGF IN LIVER REGENERATION, DIFFERENTIATION AND NEOPLASIAR01CA035373 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MICHALOPOULOS, GEORGE K · 1985 to 2011
$3.8M
HGF AND HEPATOCYTES IN NEOPLASIA AND LIVER FAILURER37CA030241 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MICHALOPOULOS, GEORGE K · 1994 to 2001
$578k
CELL CULTURE AND TRANSPLANTATION OF HUMAN HEPATOCYTESR01CA030241 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MICHALOPOULOS, GEORGE K · 1985 to 1993
–
NCI NIH HHS CA30241NCI NIH HHS CA35373NCI NIH HHS R01 CA035373
6 · The paper itself

Abstract

Hepatocyte growth factor/scatter factor (HGF/SF) is a multifunctional cytokine that is involved in many normal as well as pathological conditions. HGF/NK1, a splice variant of HGF/SF, has been reported to have either antagonistic or agonistic effects with regard to c-Met signaling depending on the cell type. In these experiments, we have determined that HGF/NK1 is a potent mitogen for rat hepatocytes in culture. Furthermore, we have found that coagulation factor Xa (fXa) is capable of cleaving HGF/NK1 and single chain HGF/SF (scHGF/SF). The products resulting from cleavage of HGF/NK1 or scHGF/SF by fXa appear as single bands under non-reducing conditions. The reaction products from the digestion of HGF/NK1 by fXa were separated under reducing conditions, and the cleavage site, as determined by N-terminal sequencing, was located C-terminal to arginine 134. Previous work established that the heparin-binding domain for HGF/SF is located in the N domain of HGF/SF. Additionally, the dimerization of the HGF/SF receptor (c-Met) by the ligand HGF/NK1 is facilitated by heparin and related sulfonated sugars on the cell surface, whereas heparin is not required for HGF/SF-mediated dimerization. Cleavage of single chain HGF/SF or HGF/NK1 by factor Xa does not alter the affinity of the respective molecules for heparin, but it did variably affect the associated mitogenic activity of these factors. The associated mitogenic activity of HGF/NK1 was reduced by more than 90%, whereas the mitogenic activity of scHGF/SF was unaffected. This suggests mandatory maintenance of a steric interaction of the N domain and the first kringle domain for HGF/NK1 to act as an agonist for rat hepatocyte growth but is not required by full-length HGF/SF.

Indexed as

Alternative SplicingMitogensAnimalsArginineBinding SitesCells, CulturedDimerizationDose-Response Relationship, DrugFactor XaHeparinHepatocyte Growth FactorHepatocytesLigandsMaleModels, MolecularProtein BindingArginineFactor XaHeparinHepatocyte Growth FactorLigandsMitogensProtein Isoforms

Identifiers

PMID11832492
PMCPMC1821081
OpenAlexW2042326648

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.