Ask about this productRelated genes to: CRABP2 Blocking Peptide
- 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 Blocking Peptide
Related articles to: CRABP2 Blocking Peptide
- 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 - - 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 - The gene, a recently identified regulator of embryonic development and stem cell pluripotency, is essential for embryonic survival, as its homozygous knockout () leads to lethality in mice at approximately embryonic day 12.5 (E12.5). To elucidate the underlying lethal mechanism, an integrated approach combining morphological observation, multi-stage transcriptomic analysis, and functional validation experiments was employed to systematically investigate the developmental disorders caused by deficiency. Morphological observation showed that / embryos exhibited significant abnormalities at developmental stages E9.0, E9.5, E10.0, E10.5, and E11.0, including shortened body axis, defective neural tube closure, aberrant somite differentiation, and cardiovascular malformations, accompanied by overall developmental delay. At the molecular level, through RNA sequencing and qRT-PCR validation revealed that deficiency not only suppressed the expression of genes critical for somitogenesis (, ), neurodevelopment (, ), and the hematopoietic system (, ), but also aberrantly activated genes associated with apoptosis (, ) and lipid metabolism (, ). TUNEL staining showed that the level of apoptosis was significantly increased in embryos. Meanwhile, immunofluorescence detection of Hif-1α indicated that the hypoxic stress response was aberrantly activated. Furthermore, the widespread dysregulation of genes involved in thyroid hormone transport (), DNA damage stress (), and lipid metabolism (, ) collectively exacerbated the developmental imbalance, ultimately leading to embryonic death. A cross-species analysis demonstrated that knockdown in human embryonic stem cells (hESCs) significantly suppressed the expression of core angiogenic genes (, and ), a finding consistent with public database analyses indicating a strong association between and the hypoxic response. In conclusion, this study elucidates that functions as a regulatory gene that maintains embryonic homeostasis by orchestrating multiple key developmental processes, including somitogenesis, neural differentiation, angiogenesis, and the hypoxic stress response. This discovery not only deepens the understanding of the role of in embryonic development but also provides a new perspective for deciphering the pathogenesis of related hereditary diseases. - Source: PubMed
Deng Ya-XinDing Bao-JunLi Hong-ChunChen SongZhang YingZhou BoZhang Zhen - This study aimed to evaluate FOXC1-mediated regulatory mechanisms on gene and protein expression profiles in primary human limbal epithelial cells (pLECs) using siRNA-mediated FOXC1 knockdown under basal conditions and following lipopolysaccharide (LPS) and interleukin-1β (IL-1β)-induced inflammatory conditions. The gene expression related to inflammation, epithelial differentiation, cell proliferation and remodeling, and retinoic acid metabolism was analyzed using qPCR. Corresponding protein levels were assessed through Western blotting and ELISA. FOXC1 silencing significantly downregulated epithelial differentiation markers KRT12 and KRT13 at the mRNA and protein levels ( ≤ 0.045), whereas KRT3 and KRT19 were unaffected. Inflammatory signaling was markedly altered, with a reduced and mRNA expression ( ≤ 0.029), increased IL-1α expression ( ≤ 0.015), and condition-dependent changes in IL-6 and IL-8 protein secretion. was increased at the mRNA level only ( = 0.007). mRNA was consistently reduced ( ≤ 0.022) without corresponding protein changes, while TGF-β protein was increased under non-inflammatory and LPS conditions ( ≤ 0.011). Genes involved in retinoid metabolism, including , , , , , and , were significantly downregulated ( ≤ 0.037), with reduced CRABP2 and RDH10 protein levels ( ≤ 0.017) and a decreased FABP5/CRABP2 ratio under IL-1β stimulation ( = 0.006). FOXC1 knockdown affected proliferation-related genes, with decreased ( = 0.048) and increased ( = 0.006). FOXC1 silencing disrupts epithelial differentiation, inflammatory signaling, retinoid metabolism, and selected proliferation-related pathways at the transcriptional level, with more selective effects on protein levels. Such changes may potentially predispose the ocular surface to lineage instability, fibrosis, and impaired regenerative capacity. - Source: PubMed
Publication date: 2026/02/15
Kundu SwarnaliAmini MaryamStachon TanjaFries Fabian NorbertSeitz BertholdLi ZhenLi ShuailinLiu ShanheHsu Shao-LunSuiwal ShwetaSzentmáry Nóra