Evidence map›Paper›PMID 7545030›Full record

ArticleMolecular biology of the cell1995

Delineation of the endocytic pathway of substance P and its seven-transmembrane domain NK1 receptor.

E F Grady, A M Garland, P D Gamp, M Lovett, D G Payan, N W Bunnett

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 207 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Inflammation and Organ Injury the Role of Substance P and Its Receptors.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Neuropeptide substance P and the immune response.Cellular and molecular life sciences : CMLS · 2016
    Review
  18. Article
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

E F GradyDepartment of Surgery, University of California, San Francisco 94143, USA.
A M Garland
P D Gamp
M Lovett
D G Payan
N W Bunnett
University of California, San Francisco · US

Funding

REGULATION OF CELLULAR RESPONSES TO NEUROPEPTIDESR37DK039957 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BUNNETT, NIGEL W · 2000 to 2010
$3.2M
REGULATION OF SIGNALING BY CELL SURFACE PROTEOLYSISR01DK043207 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BUNNETT, NIGEL W · 1993 to 2011
$1.7M
REGULATION OF SIGNALING BY CELL-SURFACE PROTEOLYSISR56DK043207 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BUNNETT, NIGEL W · 2010 to 2010
$348k
REGULATION OF CELLULAR RESPONSES TO NEUROPEPTIDESR01DK039957 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI BUNNETT, NIGEL W · 1987 to 1998
–
MODULATION OF LYMPHOCYTE FUNCTION BY SUBSTANCE PR01NS021710 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI PAYAN, DONALD G · 1985 to 1997
–
NIDDK NIH HHS DK-39957NIDDK NIH HHS DK-43207NINDS NIH HHS NS 21710
6 · The paper itself

Abstract

Many of the actions of the neuropeptide substance P (SP) that are mediated by the neurokinin 1 receptor (NK1-R) desensitize and resensitize, which may be associated with NK1-R endocytosis and recycling. We delineated this endocytic pathway in transfected cells by confocal microscopy using cyanine 3-SP and NK1-R antibodies. SP and the NK1-R were internalized into the same clathrin immunoreactive vesicles, and then sorted into different compartments. The NK1-R was colocalized with a marker of early endosomes, but not with markers of late endosomes or lysosomes. We quantified the NK1-R at the cell surface by incubating cells with an antibody to an extracellular epitope. After exposure to SP, there was a loss and subsequent recovery of surface NK1-R. The loss was prevented by hypertonic sucrose and potassium depletion, inhibitors of clathrin-mediated endocytosis. Recovery was independent of new protein synthesis because it was unaffected by cycloheximide. Recovery required endosomal acidification because it was prevented by an H(+)-ATPase inhibitor. The fate of internalized 125I-SP was examined by chromatography. SP was intact at the cell surface and in early endosomes, but slowly degraded in perinuclear vesicles. We conclude that SP induces clathrin-dependent internalization of the NK1-R. The SP/NK1-R complex dissociates in acidified endosomes. SP is degraded, whereas the NK1-R recycles to the cell surface.

Indexed as

AnimalsCell Line, TransformedCell MembraneClathrinCoated VesiclesEndocytosisEndosomesEpitopesHydrogen-Ion ConcentrationOligopeptidesPeptidesPotassiumProtein Synthesis InhibitorsProton-Translocating ATPasesRatsReceptor, IGF Type 2ClathrinEpitopesFLAG peptideOligopeptidesPeptidesPotassiumProtein Synthesis InhibitorsProton-Translocating ATPasesReceptor, IGF Type 2Receptors, Neurokinin-1Receptors, TransferrinSubstance PSucrose

Identifiers

PMID7545030
PMCPMC301212
OpenAlexW2082614214

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.