Evidence map›Paper›PMID 19605562›Full record

ArticleMolecular biology of the cell2009

The insulin-like growth factor (IGF)-I E-peptides modulate cell entry of the mature IGF-I protein.

Lindsay A Pfeffer, Becky K Brisson, Hanqin Lei, Elisabeth R Barton

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Ablation of specific insulin-like growth factor I forms reveals the importance of cleavage for regenerative capacity and glycosylation for skeletal muscle storage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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  14. Complexin activates exocytosis of distinct secretory vesicles controlled by different synaptotagmins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
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  18. Deletion of muscle GRP94 impairs both muscle and body growth by inhibiting local IGF production.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
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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.

Lindsay A PfefferDepartment of Anatomy and Cell Biology, School of Dental Medicine, and Pennsylvania Muscle Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
Becky K Brisson
Hanqin Lei
Elisabeth R Barton
University of Pennsylvania · US

Funding

IGF-I isoforms: a source for new agents to counter muscular dystrophy pathologyR21AR056480 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI BARTON, ELISABETH R · 2008 to 2009
$381k
NIAMS NIH HHS R21 AR-056480NIAMS NIH HHS R21 AR056480
6 · The paper itself

Abstract

Insulin-like growth factor (IGF)-I is a critical protein for cell development and growth. Alternative splicing of the igf1 gene gives rise to multiple isoforms. In rodents, proIGF-IA and proIGF-IB have different carboxy-terminal extensions called the E-peptides (EA and EB) and upon further posttranslational processing, produce the identical mature IGF-I protein. Rodent EB has been reported to have mitogenic and motogenic effects independent of IGF-I. However, effects of EA or EB on mature IGF-I, or whether proIGF-IA and proIGF-IB have different properties, have not been addressed. To determine whether the presence of EA or EB affected the distribution and stability of mature IGF-I protein, transient transfections of cDNAs encoding murine IGF-IA, IGF-IB, and mature IGF-I were performed in C2C12 cells, a skeletal muscle cell line. IGF-I secretion was measured by enzyme-linked immunosorbent assay of the media, and did not differ between expression of proIGF-IA, proIGF-IB, or mature IGF-I expression. Next, epitope-tagged constructs were transfected to determine cellular distribution of IGF-I, EA, and EB in the cells throughout the culture. IGF-I was detected in significantly fewer nontransfected cells in cultures transfected with mature IGF-I compared with transfection of proIGF-IA or proIGF-IB. These results demonstrate that EA and EB are not required for IGF-I secretion but that they increase cell entry of IGF-I from the media. This study provides evidence that the EA and EB may modulate IGF-I in addition to having independent activity.

Indexed as

AnimalsCell LineEndocytosisHumansInsulin-Like Growth Factor IMicePeptide FragmentsProtein IsoformsProtein PrecursorsTransfectionInsulin-Like Growth Factor IPeptide FragmentsProtein IsoformsProtein Precursors

Identifiers

PMID19605562
PMCPMC2735480
OpenAlexW2163416924

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.