Evidence map›Paper›PMID 10779334›Full record

ArticleMolecular and cellular biology2000

Deficient gene expression in protein kinase inhibitor alpha Null mutant mice.

E A Gangolli, M Belyamani, S Muchinsky, A Narula, K A Burton, G S McKnight, M D Uhler, R L Idzerda

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. RIIβ-PKA in GABAergic Neurons of Dorsal Median Hypothalamus Governs White Adipose Browning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  3. Protein kinase A inhibitor proteins (PKIs) divert GPCR-Gαs-cAMP signaling toward EPAC and ERK activation and are involved in tumor growth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
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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

8 authors at 4 institutions in 2 countries.

E A GangolliDepartment of Medicine, Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle, Washington 98195, USA.
M Belyamani
S Muchinsky
A Narula
K A Burton
G S McKnight
M D Uhler
R L Idzerda
University of Washington · USVA Puget Sound Health Care System · USInstitute of Nutrition, Metabolism and Diabetes · CAUniversity of Michigan · US

Funding

Diabetes, Obesity and Metabolism Training ProgramT32DK007247 · NIDDK · UNIVERSITY OF WASHINGTON · PI GREGORY J MORTON, KRISTINA Marie UTZSCHNEIDER · 1986 to 2026
$10.0M
REGULATION OF CYCLIC AMP-DEPENDENT PROTEIN KINASE GENESR01GM032875 · NIGMS · UNIVERSITY OF WASHINGTON · PI MCKNIGHT, GEORGE STANLEY · 1985 to 2017
$6.0M
GENETIC MUTATIONS OF PROTEIN KINASE INHIBITORR29HD033057 · NICHD · UNIVERSITY OF WASHINGTON · PI IDZERDA, REJEAN L · 1996 to 2000
$92k
NICHD NIH HHS HD 33057NIDDK NIH HHS T32 DK007247NIDDK NIH HHS T32 DK07247NIGMS NIH HHS GM 32875NIGMS NIH HHS R01 GM032875
6 · The paper itself

Abstract

Protein kinase inhibitor (PKI) is a potent endogenous inhibitor of the cyclic AMP (cAMP)-dependent protein kinase (PKA). It functions by binding the free catalytic (C) subunit with a high affinity and is also known to export nuclear C subunit to the cytoplasm. The significance of these actions with respect to PKI's physiological role is not well understood. To address this, we have generated by homologous recombination mutant mice that are deficient in PKIalpha, one of the three isoforms of PKI. The mice completely lack PKI activity in skeletal muscle and, surprisingly, show decreased basal and isoproterenol-induced gene expression in muscle. Further examination revealed reduced levels of the phosphorylated (active) form of the transcription factor CREB (cAMP response element binding protein) in the knockouts. This phenomenon stems, at least in part, from lower basal PKA activity levels in the mutants, arising from a compensatory increase in the level of the RIalpha subunit of PKA. The deficit in gene induction, however, is not easily explained by current models of PKI function and suggests that PKI may play an as yet undescribed role in PKA signaling.

Indexed as

Intracellular Signaling Peptides and ProteinsAnimalsCarrier ProteinsCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinEnzyme InhibitorsGene Expression RegulationHomozygoteIsoproterenolMiceMice, KnockoutMuscle, SkeletalPhosphorylationProtein IsoformsSignal TransductionCarrier ProteinsCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinEnzyme InhibitorsIntracellular Signaling Peptides and ProteinsIsoproterenolPkia protein, mouseProtein Isoforms

Identifiers

PMID10779334
PMCPMC85637
OpenAlexW2136114404

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.