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
- Arachnoiditis develops from inflammatory processes in the intrathecal space and can cause syringomyelia, myelopathy, radiculopathy, and chronic pain. Understanding inflammatory and fibrotic mechanisms may identify therapeutic targets. We performed a retrospective study of 60 adults who had undergone surgery for arachnoiditis-associated syringomyelia. Clinical status was assessed preoperatively and at 3 to 4 months post-surgery. Cerebrospinal fluid (CSF) was obtained preoperatively, 1-week post-operatively, and at 3 to 4 months. Operative arachnoid adhesion specimens underwent histopathologic review and immunofluorescence staining with quantitative assessment of fibrosis, inflammation, and human endogenous retrovirus group K (HERV-K) antigens. Lesions had mid-thoracic predominance and heterogeneous etiologies. Median CSF white cell counts were low preoperatively (1 cell/µL, range: 0 to 11 cells/µL). Tissue profiling supported a fibroblast-associated, scar-forming lesion (mean density of CRABP2 = 434 cells/mm2, ER-TR7 = 430 cells/mm2) with moderate collagen I deposition (8.1% of specimens), less adaptive immune signals (9 to 180 cells/mm2), and minimal HERV-K staining (1.1% of tissue). In arachnoiditis-associated syringomyelia, preoperative CSF had few white blood cells; 1-week postoperative CSF had RBC and WBC counts consistent with postoperative meningeal irritation. Chronic fibrosis characterized arachnoid tissue removed at surgery. Histology and immunohistochemical staining suggested that arachnoiditis manifested as a fibroproliferative, adhesive phenotype within the subarachnoid space. - Source: PubMed
Publication date: 2026/08/27
Choi Joseph YGraff Shantelle ANalluri Hasita VQuezado Martha MZerk Pinar EMaric DraganMcGavern Dorian BHeiss John D - Polymyositis (PM), an autoimmune muscle disorder, often leads to interstitial lung disease (ILD), including idiopathic pulmonary fibrosis (IPF). However, causality and mechanisms are unclear. This study aimed to investigate the causal effect of PM on IPF risk, identify potential mediating biomarkers through multi-omics analysis, and explore candidate therapeutic drugs. Two-sample Mendelian randomization (MR) was conducted using publicly available genome-wide association study (GWAS) summary statistics (PM: 244 cases/4,28,965 controls; IPF: 6257 cases/9,47,616 controls). Reverse-causality was evaluated via bidirectional MR. We acknowledge the potential for sample overlap between exposure and outcome datasets when using public GWAS data. To mitigate related biases, we employed robust MR methods, including inverse-variance weighted (IVW) with random effects, MR-Egger, and MR-PRESSO, that are less sensitive to such overlap. Genetic variants with significant missing data or poor imputation quality were excluded as per the quality control standards of the original GWAS. This specific analysis was not preregistered and should be considered exploratory. The analysis proceeded in two sequential phases to identify shared causal mediators: First, MR analyses were conducted with 91 inflammatory proteins, 1400 plasma metabolites, 4907 circulating proteins, and 731 immune cell traits as exposures and IPF as the outcome to identify significant causal biomarkers for IPF. Second, MR analyses were conducted with PM as the exposure and the biomarkers significantly associated with IPF as outcomes to identify those also influenced by PM with consistent effect directions. Identified key proteins underwent functional enrichment analysis. Molecular docking was used to validate interactions between significant mediators and potential drugs. PM significantly increased IPF risk (odds ratio [OR]: 1.06, 95% confidence interval [CI]: 1.02-1.09, P < .01), with no significant reverse causal evidence. Five circulating proteins (AMH, CHCHD10, CRABP2, HERC5, HSPA5) and 5 metabolites mediated this association, enriched in endoplasmic reticulum stress and transforming growth factor (TGF-β) signaling. Three drugs (butein, gambogic acid, tauroursodeoxycholic acid) showed strong binding affinity (ΔG < -7.0 kcal/mol). Genetic evidence supports PM causally increasing IPF risk. Multi-omics revealed key mediating biomarkers and underlying biological pathways, while drug target prioritization identified 3 compounds with therapeutic potential. This informs prevention strategies. - Source: PubMed
Chen MiaomiaoTong XiaZhang RuiyingZhang YazhengZhang XinLiu Bin - Cardiac fibrosis is a hallmark of ischemic heart failure and is driven by activated myofibroblasts. DNA damage and defective repair promote fibroblast activation, yet the upstream regulators that couple DNA damage responses to profibrotic remodeling remain unclear. - Source: PubMed
Publication date: 2026/07/31
Su ZhenyangShen HuiSun JinyuKong XiangqingSun Wei - Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer and remains a major cause of cancer-related mortality. Despite advances in targeted therapies, tumor heterogeneity and acquired resistance frequently undermine clinical outcomes. This study aimed to identify novel oncogenic drivers and underlying mechanisms in LUAD. - Source: PubMed
Zhu XiRuiFan BiaoFengLei QingXin ChenJunLi XuanChengMa ZhongRuiXie SiQiShang JianLiangLi ZuYangLiu ChaoWang WeiWei - Resistance to 5-fluorouracil (5-FU) necessitates its administration in combination with other drugs to enhance the clinical outcome. Oxymatrine (OMT) exhibits antitumor and anti-inflammatory activities. This study aimed to investigate the synergistic antitumor effect of OMT with 5-FU in A549 cells. - Source: PubMed
Publication date: 2026/07/25
Zeng GuofangLuo FeiZeng QiaoliWang ZhiqiangGuo Runmin