Evidence map›Paper›PMID 8978816›Full record

ArticleThe Journal of cell biology1996

Formation of nascent secretory vesicles from the trans-Golgi network of endocrine cells is inhibited by tyrosine kinase and phosphatase inhibitors.

C D Austin, D Shields

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 66 citations in OpenAlex.

  1. ADAM10 Site-Dependent Biology: Keeping Control of a Pervasive Protease.International journal of molecular sciences · 2021
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  16. Functional association between Arf and RalA in active phospholipase D complex.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  17. Protein kinase A activity is required for the budding of constitutive transport vesicles from the trans-Golgi network.Proceedings of the National Academy of Sciences of the United States of America · 1997
    Article
  18. Tetrahymena: the key to the genetic analysis of the regulated pathway of polypeptide secretion?Proceedings of the National Academy of Sciences of the United States of America · 1997
    Article
  19. 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

2 authors at 1 institution in 1 country.

C D AustinAlbert Einstein College of Medicine, Bronx, New York 10461, USA.
D Shields
Albert Einstein College of Medicine · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
IN VITRO BIOSYNTHESIS OF INSULIN AND GLUCAGONR01DK021860 · NIDDK · YESHIVA UNIVERSITY · PI CUERVO, ANA MARIA · 1986 to 2008
$5.3M
BIOSYNTHESIS AND PROCESSING OF PEPTIDE HORMONE PRECURSORR37DK021860 · NIDDK · YESHIVA UNIVERSITY · PI SHIELDS, DENNIS · 1991 to 1998
–
NCI NIH HHS P30CA13330NIDDK NIH HHS DK21860
6 · The paper itself

Abstract

Recent evidence suggests that secretory vesicle formation from the TGN is regulated by cytosolic signaling pathways involving small GTP-binding proteins, heterotrimeric G proteins, inositol phospholipid metabolism, and protein serine/threonine phosphorylation. At the cell surface, protein phosphorylation and dephosphorylation on tyrosine residues can rapidly modulate cytosolic signaling pathways in response to extracellular stimuli and have been implicated in the internalization and sorting of signaling receptors. to determine if phosphotyrosine metabolism might also regulate secretory vesicle budding from the TGN, we treated permeabilized rat pituitary GH3 cells with inhibitors of either tyrosine phosphatases or tyrosine kinases. We demonstrate that the tyrosine phosphatase inhibitors pervanadate and zinc potently inhibited budding of nascent secretory vesicles. Tyrphostin A25 (TA25) and other tyrosine kinase inhibitors also prevented secretory vesicle release, suggesting that vesicle formation requires both phosphatase and kinase activities. A stimulatory peptide derived from the NH2 terminus of the small GTP-binding protein ADP ribosylation factor 1 (ARF1) antagonized the inhibitory effect of TA25, indicating that both agents influence the same pathway leading to secretory vesicle formation. Antiphosphotyrosine immunoblotting revealed that protein tyrosine phosphorylation was enhanced after treatment with tyrosine phosphatase or kinase inhibitors. Subcellular fractionation identified several tyrosine phosphorylated polypeptides of approximately 175, approximately 130, and 90-110 kD that were enriched in TGN-containing Golgi fractions and tightly membrane associated. The phosphorylation of these polypeptides correlated with inhibition of vesicle budding. Our results suggest that in endocrine cells, protein tyrosine phosphrylation and dephosphorylation are required for secretory vesicle release from the TGN.

Indexed as

TyrphostinsADP-Ribosylation Factor 1ADP-Ribosylation FactorsAmino Acid SequenceAnimalsEnzyme InhibitorsGolgi ApparatusGTP-Binding ProteinsHumansMembrane ProteinsMolecular Sequence DataNitrilesPhosphorylationPhosphotyrosinePituitary GlandProtein-Tyrosine KinasesADP-Ribosylation Factor 1ADP-Ribosylation FactorsEnzyme InhibitorsGTP-Binding ProteinsMembrane ProteinsNitrilespervanadatePhosphotyrosineProtein-Tyrosine KinasesProtein Tyrosine PhosphatasesTyrosinetyrphostin 25TyrphostinsVanadatesZinc

Identifiers

PMID8978816
PMCPMC2133953
OpenAlexW2113111267

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.