CRABP1 in Non-Canonical Activities of Retinoic Acid in Health and Diseases

Jennifer Nhieu; Yu Lung Lin; Li Na Wei

doi:10.3390/nu14071528

CRABP1 in Non-Canonical Activities of Retinoic Acid in Health and Diseases

Jennifer Nhieu, Yu Lung Lin, Li Na Wei

Pharmacology

Research output: Contribution to journal › Review article › peer-review

5 Scopus citations

Abstract

In this review, we discuss the emerging role of Cellular Retinoic Acid Binding Protein 1 (CRABP1) as a mediator of non-canonical activities of retinoic acid (RA) and relevance to human diseases. We first discuss the role of CRABP1 in regulating MAPK activities and its implication in stem cell proliferation, cancers, adipocyte health, and neuro-immune regulation. We then discuss an additional role of CRABP1 in regulating CaMKII activities, and its implication in heart and motor neuron diseases. Through molecular and genetic studies of Crabp1 knockout (CKO) mouse and culture models, it is established that CRABP1 forms complexes with specific signaling molecules to function as RA-regulated signalsomes in a cell context-dependent manner. Gene expression data and CRABP1 gene single nucleotide polymorphisms (SNPs) of human cancer, neurodegeneration, and immune disease patients implicate the potential association of abnormality in CRABP1 with human diseases. Finally, therapeutic strategies for managing certain human diseases by targeting CRABP1 are discussed.

Original language	English (US)
Article number	1528
Journal	Nutrients
Volume	14
Issue number	7
DOIs	https://doi.org/10.3390/nu14071528
State	Published - Apr 1 2022

Bibliographical note

Funding Information:
This work is supported by NIH grants DK54733, DK60521, and the Dean?s Commitment and the Distinguished McKnight Professorship of the University of Minnesota to L.N.W., J.N. is supported by NIH fellowship F31DK123999. The authors would like to thank the ALS Variant Server (als.umassmed.edu) which is supported by funds from NIH/NINDS (1R01NS065847), AriSLA (EXOMEFALS, NOVALS), the ALS Association, and the Motor Neurone Disease Association. The results shown here are in whole or part based upon data generated by the TCGA Research Network: https://www.cancer.gov/tcga. accessed on 7 February 2022.

Publisher Copyright:
© 2022 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

CAMKII
CRABP1
MAPK
cancer
human disease
inflammation
metabolism
neurodegeneration
non-canonical
retinoic acid

PubMed: MeSH publication types

Journal Article
Review

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.3390/nu14071528

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title = "CRABP1 in Non-Canonical Activities of Retinoic Acid in Health and Diseases",

abstract = "In this review, we discuss the emerging role of Cellular Retinoic Acid Binding Protein 1 (CRABP1) as a mediator of non-canonical activities of retinoic acid (RA) and relevance to human diseases. We first discuss the role of CRABP1 in regulating MAPK activities and its implication in stem cell proliferation, cancers, adipocyte health, and neuro-immune regulation. We then discuss an additional role of CRABP1 in regulating CaMKII activities, and its implication in heart and motor neuron diseases. Through molecular and genetic studies of Crabp1 knockout (CKO) mouse and culture models, it is established that CRABP1 forms complexes with specific signaling molecules to function as RA-regulated signalsomes in a cell context-dependent manner. Gene expression data and CRABP1 gene single nucleotide polymorphisms (SNPs) of human cancer, neurodegeneration, and immune disease patients implicate the potential association of abnormality in CRABP1 with human diseases. Finally, therapeutic strategies for managing certain human diseases by targeting CRABP1 are discussed.",

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author = "Jennifer Nhieu and Lin, {Yu Lung} and Wei, {Li Na}",

note = "Funding Information: This work is supported by NIH grants DK54733, DK60521, and the Dean?s Commitment and the Distinguished McKnight Professorship of the University of Minnesota to L.N.W., J.N. is supported by NIH fellowship F31DK123999. The authors would like to thank the ALS Variant Server (als.umassmed.edu) which is supported by funds from NIH/NINDS (1R01NS065847), AriSLA (EXOMEFALS, NOVALS), the ALS Association, and the Motor Neurone Disease Association. The results shown here are in whole or part based upon data generated by the TCGA Research Network: https://www.cancer.gov/tcga. accessed on 7 February 2022. Publisher Copyright: {\textcopyright} 2022 by the authors. Licensee MDPI, Basel, Switzerland.",

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N2 - In this review, we discuss the emerging role of Cellular Retinoic Acid Binding Protein 1 (CRABP1) as a mediator of non-canonical activities of retinoic acid (RA) and relevance to human diseases. We first discuss the role of CRABP1 in regulating MAPK activities and its implication in stem cell proliferation, cancers, adipocyte health, and neuro-immune regulation. We then discuss an additional role of CRABP1 in regulating CaMKII activities, and its implication in heart and motor neuron diseases. Through molecular and genetic studies of Crabp1 knockout (CKO) mouse and culture models, it is established that CRABP1 forms complexes with specific signaling molecules to function as RA-regulated signalsomes in a cell context-dependent manner. Gene expression data and CRABP1 gene single nucleotide polymorphisms (SNPs) of human cancer, neurodegeneration, and immune disease patients implicate the potential association of abnormality in CRABP1 with human diseases. Finally, therapeutic strategies for managing certain human diseases by targeting CRABP1 are discussed.

AB - In this review, we discuss the emerging role of Cellular Retinoic Acid Binding Protein 1 (CRABP1) as a mediator of non-canonical activities of retinoic acid (RA) and relevance to human diseases. We first discuss the role of CRABP1 in regulating MAPK activities and its implication in stem cell proliferation, cancers, adipocyte health, and neuro-immune regulation. We then discuss an additional role of CRABP1 in regulating CaMKII activities, and its implication in heart and motor neuron diseases. Through molecular and genetic studies of Crabp1 knockout (CKO) mouse and culture models, it is established that CRABP1 forms complexes with specific signaling molecules to function as RA-regulated signalsomes in a cell context-dependent manner. Gene expression data and CRABP1 gene single nucleotide polymorphisms (SNPs) of human cancer, neurodegeneration, and immune disease patients implicate the potential association of abnormality in CRABP1 with human diseases. Finally, therapeutic strategies for managing certain human diseases by targeting CRABP1 are discussed.

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CRABP1 in Non-Canonical Activities of Retinoic Acid in Health and Diseases

Abstract

Bibliographical note

Keywords

PubMed: MeSH publication types

UN SDGs

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