CRABP2,1_138aa, Human Recombinant, E.coli
- Known as:
- CRABP2,1_138aa, Human Recombinant, E.coli
- Catalog number:
- RBP0801
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- CRABP2 1_138aa Human Recombinant .coli
Related genes to: CRABP2,1_138aa, Human Recombinant, E.coli
- 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
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
Related products to: CRABP2,1_138aa, Human Recombinant, E.coli
Related articles to: CRABP2,1_138aa, Human Recombinant, E.coli
- Lung cancer is the leading cause of cancer-related mortality worldwide, with LUAD being characterized by high incidence and mortality rates. Despite the use of various treatments, including surgery, chemotherapy, immunotherapy, and molecular targeted therapy, the prognosis in LUAD patients remains unfavorable. As a result, the diagnosis and management of LUAD still present major challenges. There is an urgent need to identify novel therapeutic targets. In this study, we analyzed to explore single-cell transcriptomic data (GSE253013 dataset) to investigate epithelial cells heterogeneity in LUAD. Tumor-specific epithelial subpopulations were identified, and the signature genes were evaluated for prognostic, diagnostic potential across several GEO datasets. Functional assays were conducted to validate the role of CRABP2 in lung cancer cells. Xenograft mouse models, rescue experiments and mechanistic analyzes involving ATRA-RAR signaling were further performed to elucidate the molecular mechanism. CRABP2 expression was positively correlated with MDK in LUAD. Functional assays demonstrated that CRABP2 promoted cell proliferation, migration, invasion, and vasculogenic mimicry through activation of the MDK/VEGF/MMP2/9/AKT signaling axis. In vivo xenograft experiments further confirmed that CRABP2 knockdown suppressed tumor growth and angiogenesis. Rescue experiments identified MDK as a critical downstream effector of CRABP2. Mechanistically, CRABP2 enhanced MDK transcription via activation of the ATRA-RAR signaling pathway and increased RARA occupancy at the MDK promoter. Clinically, elevated CRABP2 expression was associated with poor prognosis and showed strong diagnostic performance in LUAD. Collectively, our findings identify CRABP2-ATRA-RAR-MDK signaling axis that drives LUAD progression and angiogenesis. CRABP2 promotes MDK transcription through activation of RAR signaling, thereby enhancing malignant phenotypes and vasculogenic mimicry. These results establish CRABP2 as a promising diagnostic and prognostic biomarker and suggest that targeting the CRABP2-MDK axis may represent a potential therapeutic strategy for LUAD. - Source: PubMed
Publication date: 2026/07/19
Zhang JingshunZhang CuiJiang GuopengLiu XiaLi YifanWang FumanSun XuefeiSun Peidao - Lung adenocarcinoma (LUAD) molecular heterogeneity limits traditional prognostic models. Given the emerging role of neural regulation (NR) in tumor progression, we aimed to delineate NR-associated cellular phenotypes via single-cell RNA sequencing (scRNA-seq) and develop a robust machine-learning-derived signature (NR.Sig) to precisely assess prognosis and guide personalized immunotherapy. - Source: PubMed
Publication date: 2026/07/02
Zheng YipingMiao XiayeWang YuminWei ShuzhenZhang Qing - - Source: PubMed
International BioMed Research - 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