Evidence map›Paper›PMID 24700589›Full record

ReviewHepatology (Baltimore, Md.)2014

Role of protein kinase C isoforms in bile formation and cholestasis.

M Sawkat Anwer

Open access · bronzeAbstract readReview
In one paragraph

Review in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Hepatic protein kinase Cβ antagonizing p38American journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Molecular Regulation of Canalicular ABC Transporters.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Nonalcoholic Steatohepatitis Modulates Membrane Protein Retrieval and Insertion Processes.Drug metabolism and disposition: the biological fate of chemicals · 2016
    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

1 author at 1 institution in 1 country.

M Sawkat AnwerDepartment of Biomedical Sciences, Cummings School of Veterinary Medicine at Tufts University, North Grafton, MA.
Tufts University · US

Funding

MECHANISM OF CANALICULAR BILE FORMATION AND CHOLESTASISR01DK033436 · NIDDK · TUFTS UNIVERSITY BOSTON · PI ANWER, MOHAMMED SAWKAT · 1986 to 2010
$4.0M
Role of Protein Kinase C in Isoforms in Bile formation and CholestasisR01DK090010 · NIDDK · TUFTS UNIVERSITY BOSTON · PI ANWER, MOHAMMED SAWKAT · 2010 to 2014
$2.5M
NIDDK NIH HHS DK033436NIDDK NIH HHS DK090010NIDDK NIH HHS R01 DK033436NIDDK NIH HHS R01 DK090010
6 · The paper itself

Abstract

Transhepatic solute transport provides the osmotic driving force for canalicular bile formation. Choleretic and cholestatic agents affect bile formation, in part, by altering plasma membrane localizations of transporters involved in bile formation. These short-term dynamic changes in transporter location are highly regulated posttranslational events requiring various cellular signaling pathways. Interestingly, both choleretic and cholestatic agents activate the same intracellular signaling kinases, such as phosphoinositide-3-kinase (PI3K), protein kinase C (PKC), and mitogen-activated protein kinase (MAPK). An emerging theme is that choleretic and cholestatic effects may be mediated by different isoforms of these kinases. This is most evident for PKC-mediated regulation of plasma membrane localization of Na+-taurocholate cotransporting polypeptide (NTCP) and multidrug resistance-associated protein 2 (MRP2) by conventional PKCα (cPKCα), novel PKCδ (nPKCδ), nPKCε, and atypical PKCζ (aPKCζ). aPKCζ may mediate choleretic effects by inserting NTCP into the plasma membrane, and nPKCε may mediate cholestatic effects by retrieving MRP2 from the plasma membrane. On the other hand, cPKCα and nPKCδ may be involved in choleretic, cholestatic, and anticholestatic effects by inserting, retrieving, and inhibiting retrieval of transporters, respectively. The effects of PKC isoforms may be mediated by phosphorylation of the transporters, actin binding proteins (radixin and myristoylated alanine-rich C kinase substrate), and Rab proteins. Human NTCP plays an important role in the entry of hepatitis B and D viruses into hepatocytes and consequent infection. Thus, PKCs, by regulating NTCP trafficking, may also play an important role in hepatic viral infections.

Indexed as

AnimalsBileCholestasisHumansProtein IsoformsProtein Kinase CProtein IsoformsProtein Kinase C

Identifiers

PMID24700589
PMCPMC4141907
OpenAlexW2117021291

What OpenQuestion holds

Textmetadata
LicenceTDM
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.