Ask about this productRelated genes to: CRABP2 antibody
- Gene:
- CRABP2 NIH gene
- Name:
- cellular retinoic acid binding protein 2
- Previous symbol:
- -
- Synonyms:
- CRABP-II
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-25
- Date modifiied:
- 2016-10-05
Related products to: CRABP2 antibody
Related articles to: CRABP2 antibody
- Cadmium (Cd) is a toxic heavy metal strongly implicated in lung adenocarcinoma (LUAD) through mechanisms involving oxidative stress, epigenetic dysregulation, and chronic inflammation. This study aimed to identify Cd-responsive genes associated with LUAD and to evaluate the protective effects of oxyresveratrol (O-RES) against Cd-induced molecular alterations. Using an integrated bioinformatics approach across six GEO datasets, key differentially expressed genes (DEGs) were identified and subsequently validated in silico and in vivo using a Cd-induced rat lung injury model. DEG analysis revealed four hub genes: Cbx2, Cdh3, Crabp2, and Slc15a3, linked to chromatin remodeling, cell adhesion, retinoid signaling, and immune regulation. Cd exposure significantly dysregulated these genes and increased pro-inflammatory cytokine expression, whereas O-RES treatment dose-dependently restored gene expression and attenuated inflammation. Molecular docking further supported favorable interactions between O-RES and the hub proteins. In addition, machine learning-based regression models were applied to integrate transcriptional responses across experimental groups. A Random Forest model achieved high predictive accuracy for a Cd-O-RES exposure index (R = 0.90), while SHAP analysis identified Egln3 as the dominant context-dependent contributor, followed by Cbx2 and Crabp2. Complementary Elastic Net regression supported these findings through consistent linear associations. Overall, integrating interpretable machine learning with experimental evidence enhances mechanistic insight into Cd-induced transcriptional reprogramming and supports the protective role of O-RES. - Source: PubMed
Publication date: 2026/05/12
Isıyel MuratCeylan HamidDemir Yeliz - Congenital aniridia, a rare disorder caused by PAX6 haploinsufficiency, is characterized by progressive, vision-threatening aniridia-associated keratopathy (AAK) with limbal epithelial dysfunction and chronic inflammation. Downregulation of fatty acid binding protein 5 (FABP5) has been reported in conjunctival cells of congenital aniridia patients and in limbal epithelial cells (LECs) of the PAX6 siRNA knockdown model. We aimed to investigate the effects of FABP5 deficiency on LECs gene expression, without or with inflammatory stimuli. To achieve FABP5 knockdown, human primary LECs were transfected with FABP5 siRNA, using Lipofectamine 2000. Inflammation was induced 48 hours after transfection by incubating cells with 2 µg/mL lipopolysaccharides (LPS) or 1 ng/ml IL-1β. Thereafter, gene and protein levels were examined using qPCR, Western blot and ELISA. Significant downregulation of PAX6, KRT3 and MMP2 and upregulation of KRT12 mRNA level was observed upon FABP5 knockdown (p ≤ 0.022). Under inflammatory conditions (IL-1β or LPS treatment), FABP5 knockdown led to reduced PAX6, FOSL2, IL-6, PTGES2, KRT3, MAPK3 and MMP2 (p ≤ 0.048) and increased VEGFα and CRABP2 mRNA expression levels compared to control LECs (p ≤ 0.034). Following FABP5 knockdown, reduced PAX6, IL-6 and KRT3 protein levels were confirmed in absence of inflammatory stimuli and in cells treated with IL-1β (p ≤ 0.034). Our results suggest a novel role of FABP5 protein in AAK progression by controlling expression levels of genes and proteins involved in LEC differentiation. In addition, under inflammatory conditions, FABP5 deficiency affects key transcription factors (PAX6, FOSL2), genes regulating LEC migration, differentiation and cell maintenance (KRT3, VEGFα, MAPK3, CRABP2), and genes involved in inflammation (IL-6, PTGES2). - Source: PubMed
Publication date: 2026/04/28
Amini MaryamHsu Shao-LunStachon TanjaLi ZhenChai NingFries Fabian NSeitz BertholdKundu SwarnaliSuiwal ShwetaSzentmáry Nóra - To study the time course of the differentiation process and its regulatory networks in primary limbal epithelial cells (pLECs) using serum-free, low calcium Keratocyte growth medium 3 (KGM3) and CnT-2D differentiation medium. : pLECs were isolated from corneoscleral rims from healthy donors and cultured in serum-free low calcium (0.06 mM Ca) KGM3. Differentiation was induced by supplementation with CnT-2D differentiation medium, while control cells were maintained in low-calcium KGM3 medium. Gene and protein expression analyses were performed using qPCR and Western blotting, respectively, at 72 h and at 5, 7, 10, and 14 days post-supplementation to determine the optimal time course of differentiation induction. : CnT-2D differentiation medium supplementation resulted in a significant upregulation of differentiation-associated markers, including desmoglein 1 (DSG1), paired box domain 6 (PAX6), keratin 3 (KRT3), fatty acid binding protein 5 (FABP5), cellular retinoic acid binding protein 2 (CRABP2), alcohol dehydrogenase 7 (ADH7), aldehyde dehydrogenase 1A1 (ALDH1A1), with the most pronounced changes observed at day 10 post-supplementation ( ≤ 0.05). CnT-2D differentiation medium effectively initiates differentiation of limbal epithelial cells in vitro. The gradual increase in the expression of key differentiation markers, including DSG1, KRT3, and PAX6, indicates that CnT-2D medium successfully induces differentiation in 2D cultured primary limbal epithelial cells. However, subcellular localization of these markers, epithelial barrier function, and differentiation in 3D models were not assessed and remain to be investigated. - Source: PubMed
Publication date: 2026/04/12
Suiwal ShwetaKumar VirendraStachon TanjaKatiyar PriyaFries Fabian NSeitz BertholdLi ShuailinHsu Shao-LunLiu ShanheKundu SwarnaliAmini MaryamHäcker SabrinaSzentmáry Nóra - Microtia is a common congenital craniofacial malformation characterized by the partial or complete absence of the external ear structure. Despite its relatively high incidence, the pathogenesis of microtia remain poorly understood. In this study, we analyzed both single-cell and bulk RNA sequencing data from microtia cases and identified a population of COL1 HES1mesenchymal stem cell in perichondrium with significantly higher expression of the CRABP2 gene, a gene that encodes a nuclear transporter of retinoic acid. Gene expression analysis further confirmed that the RA signaling intensity and stemness are both higher in COL1HES1 perichondral stem cells from microtia patients, possibly due to elevated CRABP2 levels. Through histological verification we further confirmed the presence of this cell population with high CRABP2 expression in the perichondrium. Mechanistically, the elevated CRABP2 expression in perichondral stem cells seen in microtia patients may cause dysregulated RA signaling and disrupt the regulation of stem cell differentiation during auricular development. Histological analysis further revealed higher KLF2 expression as well as cartilage hypoplasia in microtia samples. Our study identified that the CRABP2-induced RA dysregulation in COL1 HES1 perichondral stem cells may contribute to microtia. These findings offer new insights into the etiology of microtia and provide potential directions for prenatal prevention and tissue engineering treatments. - Source: PubMed
Publication date: 2026/04/13
Zhang JinghengChu FeiyangHu XuzhongYang XinghuaLei ShaorongHe LerenWu DingyuLin LinJiang Haiyue - Medulloblastoma, a pediatric brain tumor, frequently features chromatin modifier mutations, including SMARCA4 loss in the aggressive Group 3 subgroup. While SMARCA4 is considered a tumor suppressor, the functional impact of its loss on the oncogenic programs in Group 3 MB remains poorly understood. Using doxycycline-inducible shRNA constructs in HD-MB03 cells (a MYC-amplified Group MB model) to achieve SMARCA4 knockdown, we applied quantitative mass spectrometry to profile the resulting proteomic changes. DIA-MS with an in-house library achieved superior proteome depth over DDA and proved optimal for detecting subtle chromatin remodeler effects. Key findings include dysregulation of multiple subunits of the SWI/SNF complex including SMARCA2 overexpression, upregulation of histones, and PRMT5 disrupting chromatin architecture. GSEA revealed cell cycle, spindle and kinetochore organization, DNA replication/repair, and amino acid catabolism to be suppressed. SMARCA4 loss also led to a striking lipid metabolism reprogramming, with steroid biosynthesis, fatty acid biosynthesis, and other peroxisomal lipid pathways being enriched. The overexpression of top candidates like SMARCA2, CRABP2, FABP5, TAGLN2, CYP27A1, and SCP2 was validated in a separate validatory set. Our study reveals the proteomic landscape of Group 3 medulloblastoma following SMARCA4 loss, highlighting novel therapeutic targets for functional validation and exploitation. - Source: PubMed
Publication date: 2026/03/26
Pai Medha Gayathri JSingh AvinashPatra SayanNarang DeepanshuBapat PurnaBharambe Harish ShrikrishnaShirsat NeelamSrivastava Sanjeeva