Evidence map›Paper›PMID 28132904›Full record

ReviewPharmacology & therapeutics2017

Cellular retinoid binding-proteins, CRBP, CRABP, FABP5: Effects on retinoid metabolism, function and related diseases.

Joseph L Napoli

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed
9.0field-weighted citation impact, top 1% 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

147 citing papers in PubMed, 250 citations in OpenAlex.

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87 more citing papers are in PubMed but not listed here.

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.

Joseph L NapoliDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, United States. Electronic address: jna@berkeley.edu.
University of California, Berkeley · US

Funding

Pre-doctoral Training in Molecular and Biochemical NutritionT32DK061918 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI NAPOLI, JOSEPH L · 2002 to 2016
$2.6M
Ethanol effects on retinoic acid function in embryo hippocampusR01AA017927 · NIAAA · UNIVERSITY OF CALIFORNIA BERKELEY · PI NAPOLI, JOSEPH L · 2009 to 2015
$2.4M
Retinoid HomeostasisR01DK102014 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI NAPOLI, JOSEPH L · 2015 to 2019
$1.7M
Function of 9-cis-retinoic acidR01DK090522 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI NAPOLI, JOSEPH L · 2011 to 2014
$1.3M
NIAAA NIH HHS R01 AA017927NIDDK NIH HHS R01 DK090522NIDDK NIH HHS R01 DK102014NIDDK NIH HHS T32 DK061918
6 · The paper itself

Abstract

Cellular binding-proteins (BP), including CRBP1, CRBP2, CRABP1, CRABP2, and FABP5, shepherd the poorly aqueous soluble retinoids during uptake, metabolism and function. Holo-BP promote efficient use of retinol, a scarce but essential nutrient throughout evolution, by sheltering it and its major metabolite all-trans-retinoic acid from adventitious interactions with the cellular milieu, and by imposing specificity of delivery to enzymes, nuclear receptors and other partners. Apo-BP reflect cellular retinoid status and modify activities of retinoid metabolon enzymes, or exert non-canonical actions. High ligand binding affinities and the nature of ligand sequestration necessitate external factors to prompt retinoid release from holo-BP. One or more of cross-linking, kinetics, and colocalization have identified these factors as RDH, RALDH, CYP26, LRAT, RAR and PPARβ/δ. Michaelis-Menten and other kinetic approaches verify that BP channel retinoids to select enzymes and receptors by protein-protein interactions. Function of the BP and enzymes that constitute the retinoid metabolon depends in part on retinoid exchanges unique to specific pairings. The complexity of these exchanges configure retinol metabolism to meet the diverse functions of all-trans-retinoic acid and its ability to foster contrary outcomes in different cell types, such as inducing apoptosis, differentiation or proliferation. Altered BP expression affects retinoid function, for example, by impairing pancreas development resulting in abnormal glucose and energy metabolism, promoting predisposition to breast cancer, and fostering more severe outcomes in prostate cancer, ovarian adenocarcinoma, and glioblastoma. Yet, the extent of BP interactions with retinoid metabolon enzymes and their impact on retinoid physiology remains incompletely understood.

Indexed as

AnimalsFatty Acid-Binding ProteinsGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansNeoplasmsReceptors, Retinoic AcidRetinoidsRetinol-Binding Proteins, CellularTretinoinFABP5 protein, humanFatty Acid-Binding ProteinsReceptors, Retinoic AcidRetinoidsRetinol-Binding Proteins, CellularTretinoinCellular retinoic acid binding-proteinCellular retinol binding-proteinRetinal dehydrogenaseRetinoic acidRetinoidsRetinolRetinol dehydrogenase

Identifiers

PMID28132904
PMCPMC5408321
OpenAlexW2582538856

What OpenQuestion holds

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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.