C5orf23
- Known as:
- C5orf23
- Catalog number:
- 003107A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- C5orf23
Ask about this productRelated genes to: C5orf23
- Gene:
- NPR3 NIH gene
- Name:
- natriuretic peptide receptor 3
- Previous symbol:
- NPRC, ANPRC, C5orf23
- Synonyms:
- GUCY2B, FLJ14054
- Chromosome:
- 5p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-27
- Date modifiied:
- 2014-11-19
Related products to: C5orf23
Related articles to: C5orf23
- Salicylic acid (SA) is a key phytohormone that activates plant defense responses . In Arabidopsis, NPR1 (also known as NIM1) and NPR3/NPR4 have been identified as dual SA receptors responsible for perceiving SA . However, the mechanisms of how SA binding to the NPR proteins leads to induction of defense gene expression remain unclear. Here, we elucidate how SA triggers transcriptional activation via NPR1 and relieves transcriptional repression mediated by NPR3/NPR4. We identified Mediator Complex Subunit 15A (MED15A) as a bridge between NPR1 and the Mediator complex governing transcription. SA induces direct interaction of NPR1 with MED15A. Structural and functional analysis showed that the binding of NPR1 to MED15A is essential for NPR1-mediated transcriptional activation. Meanwhile, SA relieves transcriptional repression mediated by NPR3/NPR4. NIM1-interacting 1 (NIMIN1) interacts with NPR3/NPR4 and the Topless (TPL) co-repressor, connecting them to Polycomb Repressive Complex 2 (PRC2) to mediate H3K27 trimethylation of SA-responsive genes. SA inhibits the interactions between NPR3/NPR4 and NIMIN1, reduces H3K27 trimethylation levels and increases histone acetylation of the target genes to release NPR3/NPR4-mediated repression. Our study offers a comprehensive view of SA-mediated defense gene activation. These findings lay a foundation for designing more effective SA analogs as agrochemicals and for engineering crop resistance by manipulating SA perception and signaling. - Source: PubMed
Publication date: 2026/09/16
Peng YujunTian HainanMing ZhenhuaSun TongjunYu JiuyangWu MingsongHuang DanyiZhang YihanZhong ZhenhuiLi XinZhang Yuelin - Papillary thyroid carcinoma (PTC) usually has a favorable prognosis, yet a subset of patients develops persistent, recurrent, or biologically aggressive disease. The clinical relevance of lysine β-hydroxybutyrylation (Kbhb)-related transcriptional programs in PTC remains unclear. Accordingly, this study aimed to characterize Kbhb-related molecular heterogeneity in PTC, construct a prognostic signature, and explore its association with the tumor microenvironment (TME). - Source: PubMed
Publication date: 2026/07/15
An XiaoxiaoLi BiaoZhai Baowei - The aldosterone-suppressing effect of natriuretic peptides (NPs) has been demonstrated in experiments using adrenocortical cells from various animal species. 3',5'-cyclic guanosine monophosphate (cGMP), which is produced by atrial natriuretic peptide (ANP), is recognized as a suppressor of aldosterone production. However, it has also been reported that cGMP does not exhibit the same aldosterone-suppressing effect as ANP. Therefore, we examined the effect of ANP on aldosterone suppression using various inhibitors and agonists, including a cGMP agonist. - Source: PubMed
Morishima NorikoIchihara AtsuhiroWatanabe DaisukeTakano NoriyoshiMorimoto SatoshiSeki Yasufumi - The cardiovascular-renal-liver-metabolic (CKLM) syndrome integrates dysmetabolically driven heart, vascular, kidney, and liver diseases through a shared pathophysiological substrate. In obesity, upregulation of the clearance natriuretic peptide receptor C (NPR-C) in adipose tissue creates a "NP deficiency," undermining the protective cardiovascular and metabolic actions of endogenous NPs. Recent preclinical data demonstrates that NPR-C functions beyond simple peptide clearance. Through interactions with ligands like CNP, musclin, and osteocrin, NPR-C triggers context-dependent intracellular signaling. In experimental models, independent of systemic NP levels, NPR-C directly modulates cardiac remodeling, podocyte injury, hepatic steatosis, vascular inflammation, and adipocyte function. This review synthesizes NPR-C biology within the CKLM framework. While human validation remains limited, targeting tissue-specific NPR-C pathways represents a promising therapeutic frontier for restoring cardiometabolic homeostasis. - Source: PubMed
Publication date: 2026/07/10
Landolfo MatteoSpannella FrancescoSalvà ChiaraRadlinger BernhardKaser SusanneGezzi AlessandroSarzani Riccardo - Osteoarthritis (OA) is a degenerative joint disease characterized by synovial inflammation, cartilage degradation, and subchondral bone remodeling. Currently, no universally accepted or clinically validated biomarkers exist for OA diagnosis and treatment, highlighting the need to identify potential genetic biomarkers to support early detection and therapeutic research. - Source: PubMed
Zheng GuihaoOuyang YulongChen ShuilinHu BeiXu ShuaiSun Guicai