C_REACTIVE PROTEIN, Rat (CRP)
- Known as:
- C_REACTIVE PROTEIN, Rat (CRP)
- Catalog number:
- 144-11
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- LeeBio
- Gene target:
- C_REACTIVE PROTEIN Rat (CRP)
Ask about this productRelated genes to: C_REACTIVE PROTEIN, Rat (CRP)
- Gene:
- ABCG2 NIH gene
- Name:
- ATP binding cassette subfamily G member 2 (Junior blood group)
- Previous symbol:
- -
- Synonyms:
- EST157481, MXR, BCRP, ABCP, CD338
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2019-04-23
- Gene:
- ADIPOQ NIH gene
- Name:
- adiponectin, C1Q and collagen domain containing
- Previous symbol:
- ACDC
- Synonyms:
- ACRP30, AdipoQ, apM1, GBP28, adiponectin
- Chromosome:
- 3q27.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-26
- Date modifiied:
- 2016-10-05
- Gene:
- BANF1P1 NIH gene
- Name:
- barrier to autointegration factor 1 pseudogene 1
- Previous symbol:
- -
- Synonyms:
- BCRP1, D14S1460, D14S1460E, BCRG1
- Chromosome:
- 14q24.1
- Locus Type:
- pseudogene
- Date approved:
- 2003-04-09
- Date modifiied:
- 2012-04-19
- Gene:
- C1QTNF4 NIH gene
- Name:
- C1q and TNF related 4
- Previous symbol:
- -
- Synonyms:
- CTRP4, ZACRP4
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-02
- Date modifiied:
- 2017-03-01
- Gene:
- C1QTNF6 NIH gene
- Name:
- C1q and TNF related 6
- Previous symbol:
- -
- Synonyms:
- CTRP6, ZACRP6
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-02
- Date modifiied:
- 2017-03-01
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- MicroRNA(miRNAs) are key post-transcriptional regulators of gene expression and play a role in body color formation in aquatic animals. However, their functional roles in body color formation in Chinese soft-shelled turtle (Pelodiscus sinensis) remain largely uncharacterized. Here, we combined in vitro and in vivo approaches to dissect the regulatory mechanisms of miR-18a-3p_3 and miR-221 on pigmentation-related genes. Dual-luciferase reporter assays confirmed direct binding between miR-18a-3p_3 and the 3'UTR of Sox10, as well as between miR-221 and Mitf. Mutations in the predicted binding sites abolished these interactions, validating the specificity of targeting. Subsequently, we successfully isolated and cultured melanocytes from P. sinensis embryos using a specialized medium, enabling functional validation of miRNA effects on pigmentation gene expression. Transfection of miR-18a-3p_3 antagomir and miR-221 agomir into primary melanocytes modulated the expression of Sox10 and Mitf, respectively, and altered the transcription of downstream melanogenic genes including Tyr, Tyrp1, and Gpnmb. In vivo administration of miRNA modulators (antagomir/agomir) confirmed these regulatory patterns in turtle tissues, though tissue-specific expression differences were less pronounced than in cultured cells, suggesting context-dependent regulatory complexity. Collectively, we speculated that miR-18a-3p_3 might be negatively modulating Sox10, while miR-221 positively regulated Mitf, thereby coordinating melanin synthesis in P. sinensis. These findings provide novel insights into the molecular basis of body color variation in turtles and expand our understanding of miRNA-mediated pigmentation regulation in aquatic vertebrates. - Source: PubMed
Publication date: 2026/04/26
Wang PeiGei LingruiZeng DanWang ZiaoQin QinHu YazhouWang Xiaoqing - Melanotic schwannoma (MS) is a rare peripheral nerve sheath tumor accompanied by melanin deposition and severe refractory pain. However, its molecular pathogenesis remains unclear. This study aimed to explore the histomorphological, transcriptomic, and proteomic characteristics of MS, and to identify key molecules related to melanin production, pain generation, and targeted therapy. - Source: PubMed
Publication date: 2026/04/17
Jiang YiZhao RuiXian HangShi LinZhang Jin-KangLi Song-LinPeng YeDu Jun-JieCong RuiWang Han - Tyrosinase promotes excessive deposition of melanin, which may lead to severe skin diseases. seeds have been reported to be rich in diverse bioactive constituents exhibiting potential tyrosinase inhibitory activity. However, the principal bioactive constituents responsible for tyrosinase inhibitory activity and its underlying mechanisms remain largely unclear. Therefore, this study aimed to: (1) optimize SC-CO extraction of seed oil (PFSO) for maximum yield and bioactive preservation; (2) comprehensively characterize its physicochemical and phytochemical profile; (3) elucidate the tyrosinase inhibition mechanism through kinetic, spectroscopic, and computational approaches; and (4) validate its safety, antioxidant, and anti-pigmentation efficacy in a zebrafish model. PFSO exhibited a yield of 24.96%, with a high content of unsaturated fatty acids (88.03%, mainly linoleic acid at 74.40%). The oil inhibited tyrosinase via a reversible mixed-type mechanism (IC = 1.12 mg/mL). Fluorescence spectroscopy and molecular docking revealed that linoleic acid binds to LYS180 and β-sitosterol binds to TYR78, mainly driven by hydrogen bonding and hydrophobic interaction, which changed the microenvironment of tryptophan residues and indicated static quenching. Further validation experiments revealed that the major constituent, linoleic acid, exhibited only weak inhibitory activity against tyrosinase (IC = 29.44 mg/mL), whereas the key component β-sitosterol markedly suppressed tyrosinase activity (IC = 46.43 μg/mL). In vitro assays demonstrated PFSO's significant efficacy in reducing the melanin content and tyrosinase activity in α-MSH-stimulated B16F10 murine melanoma cells. In vivo experiments in zebrafish that received dietary supplementation with PFSO confirmed that PFSO (≤5 mg/mL) reduced ROS production, suppressed melanin deposition, inhibited tyrosinase activity, and downregulated the expression of melanogenesis-related genes (TYR, TYRP1, TYRP2, MITF). This study provides, for the first time, a comprehensive elucidation of PFSO's potential as a natural tyrosinase inhibitor, integrating extraction optimization, multicomponent characterization, multimodal inhibition analysis, and in vivo validation. - Source: PubMed
Publication date: 2026/04/06
Li JingyuTao ZhihuaGuo QingquanZhang YudongZhang JunhaoDeng YanlinWu KegangYu HongpengChai XianghuaJiang YingfenHe DongLiu XiaoliDuan XuejuanLiu Junfeng - The yellow variant of the Chinese soft-shelled turtle (Pelodiscus sinensis), a product of artificial breeding, is characterized by a distinct yellow skin pigmentation and red eyes. To uncover the molecular mechanism underlying this phenotype, we employed an integrated multi-omics approach. We examined histocytological and ultrastructural differences in calipash tissues between green and yellow turtles, as well as changes in biochemical compounds associated with the yellow phenotype. We performed whole-genome resequencing, transcriptomic, and quantitative real-time PCR analyses to identify the causal mutation and to reveal differential gene expression between the two morphs. Our analyses revealed that the yellow phenotype was caused by a single non-synonymous point mutation in the tyrp1 gene. This mutation led to diminished tyrosinase expression and activity, reduced melanin synthesis, and elevated cysteine levels. These changes collectively promoted pheomelanin production at the expense of eumelanin, resulting in the yellow phenotype. Concomitantly, the downregulation of keratin-related genes suggested that reduced melanin undermined the structural integrity of the stratum corneum, resulting in its thinning. Furthermore, reduced melanin levels were associated with enhanced activation of the PI3K/AKT signaling pathway and the upregulated expression of collagen-related genes, ultimately promoting collagen production. Our findings demonstrate that the tyrp1 mutation drives the yellow phenotype by reducing melanin synthesis, an effect coupled with stratum corneum thinning and enhanced collagen deposition. Our study provides the first evidence of a mechanistic link whereby a primary defect in melanogenesis may alter both epidermal architecture and the dermal extracellular matrix. - Source: PubMed
Publication date: 2026/04/10
Zhong JunLu Yu-HongYe Jia-LingLi Jin-HangHong Ming-ShenHan Zhi-KangJi Xiang - To develop a macrophage-targeted therapy for choroidal melanoma using lipid nanoparticles (LNPs) that deliver TYRP1-CAR mRNA to reprogram tumor-associated macrophages. - Source: PubMed
Publication date: 2026/04/10
Chen WenfeiWang DongliangLi JingniLing JieLiang JiangboHu QiulingZhang QikaiZheng Ying-FengLin Xian-ChaiQu BoGuo Mengxiang