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Last update 08 May 2025

CRABP1

Last update 08 May 2025

Basic Info

Synonyms

cellular retinoic acid binding protein 1, cellular retinoic acid-binding protein 1, Cellular retinoic acid-binding protein I

+ [5]

Introduction

Cytosolic CRABPs may regulate the access of retinoic acid to the nuclear retinoic acid receptors.

Drugs associated with CRABP1

alpha-NF-ATRA

Target

CRABP1 x CRABP2

Mechanism

CRABP1 inhibitors [+1]

Active Org.-

Originator Org.

National Institute of Health Sciences

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

beta-NF-ATRA

Target

CRABP1 x CRABP2

Mechanism

CRABP1 inhibitors [+1]

Active Org.-

Originator Org.

National Institute of Health Sciences

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ITE-ATRA

Target

CRABP1 x CRABP2

Mechanism

CRABP1 inhibitors [+1]

Active Org.-

Originator Org.

National Institute of Health Sciences

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CRABP1

100 Translational Medicine associated with CRABP1

0 Patents (Medical) associated with CRABP1

651

Literatures (Medical) associated with CRABP1

01 Dec 2025·Functional & Integrative Genomics

Transcriptome analysis of the hypothalamus and testes in Brandt’s Vole: new insights into mechanisms of photoperiodic plasticity in postnatal testicular development

Article

Author: Liu, Xiao-Hui ; Ying, Yaqi ; Zhao, Lijuan ; Li, Ning ; Wang, Lewen ; Song, Ying ; Wang, Dawei ; Wang, Zhenlong ; Sun, Hong

Postnatal gonadal development is regulated by photoperiod via the hypothalamus, especially in seasonal breeding small rodents. However, the precise molecular mechanisms remain unclear. In this study, we conducted a comparative analysis of the transcriptomes of the hypothalamus and testes in 10-week-old male Brandt's voles born under long (LP, 16L:8D) and short photoperiod (SP, 8L:16D) conditions. Results indicate that the SP group exhibited significantly smaller testes with spermatogenesis halted before meiosis, identifying 129 differentially expressed genes (DEGs) in the hypothalamus and 21,673 DEGs in the testes. In the hypothalamus, genes involved in the thyroid hormone and retinoic acid (RA) pathway were notably altered under SP conditions, including decreased Tshb and Cga expression, increased Dio3, and reduced Crabp1 and Lrat, highlighting their key roles in SP signaling. In the testes, downregulated genes were significantly enriched in male reproduction-related GO terms and metabolic KEGG pathways, such as steroid hormone biosynthesis and retinol metabolism. Key genes for testosterone synthesis (e.g. Star, Cyp11a1) and RA synthesis (e.g. Rdh10, Rdh11) were downregulated, while those linked to RA degradation (Cyp26b1) and undifferentiated spermatogonia maintenance (e.g. Gdnf, Gfra1) were upregulated. These findings outline a molecular microenvironment that favors the preservation of undifferentiated spermatogonia over their differentiation from the hypothalamus to the testes. This study firstly provides valuable insights into the transcriptomic basis of SP-inhibited testicular development in Brandt's voles.

01 May 2025·Arteriosclerosis, Thrombosis, and Vascular Biology

The 9p21.3 Coronary Artery Disease Risk Locus Drives Vascular Smooth Muscle Cells to an Osteochondrogenic State

Article

Author: Miller, Clint L. ; Suryavanshi, Shraddha ; Zade, Rohan ; Lo Sardo, Valentina ; Parikh, Parth ; de Medeiros Vieira, Carolina ; Mosquera, Jose Verdezoto ; Salido, Elsa

BACKGROUND:Genome-wide association studies have identified common genetic variants at ≈300 human genomic loci linked to coronary artery disease susceptibility. Among these genomic regions, the most impactful is the 9p21.3 coronary artery disease risk locus, which spans a 60-kb gene desert and encompasses ≈80 SNPs (single nucleotide polymorphism) in high linkage disequilibrium. Despite ≈2 decades since its discovery, the role of the 9p21.3 locus in cells of the vasculature remains incompletely resolved.METHODS: We differentiated induced pluripotent stem cells (iPSCs) from risk, nonrisk donors at 9p21.3, and isogenic knockouts into vascular smooth muscle cells (VSMCs). We performed single-cell transcriptomic profiling, including coembedding and comparison with publicly available human arterial data sets. We conducted functional characterization using migration and calcification assays and confirmed our findings on iPSC–VSMCs derived from additional donors. Finally, we used overexpression of ANRIL followed by gene expression analysis. RESULTS: We demonstrated that iPSC–VSMCs harboring the 9p21.3 risk haplotype preferentially adopt an osteochondrogenic state and show remarkable similarity to fibrochondrocytes from human artery tissue. The transcriptional profile and functional assessment of migration and calcification capacity across iPSC–VSMC lines from multiple donors concordantly resemble an osteochondrogenic state. Importantly, we identified numerous transcription factors driving different VSMC state trajectories. Additionally, we prioritized LIMCH1 and CRABP1 as signature genes critical for defining the risk transcriptional program. Finally, overexpression of a short isoform of ANRIL in 9p21.3 knockout cells was sufficient to induce the osteochondrogenic transcriptional signature. CONCLUSIONS: Our study provides new insights into the mechanism of the 9p21.3 risk locus and defines its previously undescribed role in driving a disease-prone transcriptional and functional state in VSMCs concordant with an osteochondrogenic-like state. Our data suggest that the 9p21.3 risk haplotype likely promotes arterial calcification, through altered expression of ANRIL , in a cell type–specific and cell-autonomous manner, providing insight into potential risk assessment and treatment for carriers.

01 Jan 2025·Current Topics in Developmental Biology

The interplay between retinoic acid binding proteins and retinoic acid degrading enzymes in modulating retinoic acid concentrations

Review

Author: Isoherranen, Nina ; Wen, Yue Winnie

The active metabolite of vitamin A, all-trans-retinoic acid (atRA), is critical for maintenance of many cellular processes. Although the enzymes that can synthesize and clear atRA in mammals have been identified, their tissue and cell-type specific roles are still not fully established. Based on the plasma protein binding, tissue distribution and lipophilicity of atRA, atRA partitions extensively to lipid membranes and other neutral lipids in cells. As a consequence, free atRA concentrations in cells are expected to be exceedingly low. As such mechanisms must exist that allow sufficiently high atRA concentrations to occur for binding to retinoic acid receptor (RARs) and for RAR mediated signaling. Kinetic simulations suggest that cellular retinoic acid binding proteins (CRABPs) provide a cytosolic reservoir for atRA to allow high enough cytosolic concentrations that enable RAR signaling. Yet, the different CRABP family members CRABP1 and CRABP2 may serve different functions in this context. CRABP1 may reside in the cytosol as a member of a cytosolic signalosome and CRABP2 may bind atRA in the cytosol and localize to the nucleus. Both CRABPs appear to interact with the atRA-degrading cytochrome P450 (CYP) family 26 enzymes in the endoplasmic reticulum. These interactions, together with the expression levels of the CRABPs and CYP26s, likely modulate cellular atRA concentration gradients and tissue atRA concentrations in a tightly coordinated manner. This review provides a summary of the current knowledge of atRA distribution, metabolism and protein binding and how these characteristics may alter tissue atRA concentrations.

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CRABP1

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