Human Reticulocalbin-3 RCN3
- Known as:
- Human Reticulocalbin-3 RCN3
- Catalog number:
- CG56
- Product Quantity:
- l0
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Human Reticulocalbin-3 RCN3
Ask about this productRelated genes to: Human Reticulocalbin-3 RCN3
- Gene:
- RCN3 NIH gene
- Name:
- reticulocalbin 3
- Previous symbol:
- -
- Synonyms:
- RLP49
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-20
- Date modifiied:
- 2015-11-16
Related products to: Human Reticulocalbin-3 RCN3
Related articles to: Human Reticulocalbin-3 RCN3
- The lack of preventive measures for renal cell carcinoma (RCC) lung metastasis and effective treatments for metastatic RCC is currently an unmet clinical need that needs to be addressed. The DNA methylation profiling of primary RCC with matched lung metastases remains unclear, which could lead to novel biomarkers and therapeutic targets that may limit the metastasis of renal cancer. In this study, extended-representation bisulfite sequencing and transcriptome sequencing were performed on primary RCC with matched lung metastases to identify metastasis-related genes associated with DNA methylation. Among these genes, reticulocalbin 3 (RCN3) was associated with RCC progression. We found that promoter hypomethylation can upregulate the expression of RCN3. The upregulation of RCN3 can promote the malignant phenotype of RCC in vitro while promoting RCC lung metastasis in vivo. We also demonstrate that RCN3 interacts with MMP10 through its EF-hand 5-6 domains, which promotes the secretion of MMP10 and activates the PI3K/Akt pathway. Finally, we identified that Carboxy-pyridostatin 2HCl may inhibit the metastasis of RCC by binding to the pocket at the binding interface between RCN3 and MMP10. Together, these findings suggest that RCN3 is hypomethylated and upregulated in RCC lung metastasis and plays an important role in RCC lung metastasis, which may serve as a potential therapeutic target. - Source: PubMed
Publication date: 2026/04/09
Lin WenhaoWang QiXu KandiDing JiaweiMa ZhiyangXing SiweiXu DanfengHe YayiChen Lu - Despite advances in immune checkpoint blockade, resistance in metastatic melanoma remains a major challenge. To decode resistance mechanisms, we generate a comprehensive longitudinal, multi-omic, and spatial atlas of 45 tumor samples across 10 patients. Analysis reveals resistant tumors undergo convergent evolution toward a shared, spatially organized immunosuppressive ecosystem. We identify a structural mechanism characterized by spatial partitioning of immune checkpoints, where B7-H3 dominates MITF-high niches while IDO1 characterizes MITF-low zones. Furthermore, integrated single-cell and spatial analysis identifies a specific malignant subclone (c1) and a distinct architectural niche (RCN3), both exhibiting aberrant PI3K-mTOR signaling. Notably, c1 promotes the "ignored tumor" phenotype via FN1-ITGB1 and GDF15 signaling. Validated across independent cohorts, these spatial and molecular signatures predict poor survival and point to actionable targets. Ultimately, our study elucidates the spatial logic of resistance and provides a rationale for translating multi-omic discoveries into actionable, personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/03/30
Wei ShiyouDeng YulanLee JinhoLan HongbinYang ZhenyuLabrie MarilyneBetts Courtney BDuan HaoTate BenjaminPucilowska JoannaFrederick DennieLawless Aleigha RSharova TatyanaYang YuanzhongHu WanmingBeasley Georgia MSchuchter Lynn MWang XiuqiXu WeiYong GenVandenberg Megan E GTorigian Drew ASivagnanam ShamileneDu KuangSugarman EricMcGettigan SuzanneZheng CathyAl-Rohil Rami NSelim Maria ADatto Michael BLópez Giselle YNair Smita KAshley David MXu XiaoweiAmaravadi Ravi KKarakousis Giorgos CO'Rourke Donald MBrem StevenO'Malley Bert WDemirkan GokhanYu ShuangxingLu YilingCamp ToddPatterson Janice AWei ZhiCorless ChristopherGabrilovich Dmitry IMou YonggaoFlaherty Keith TCoussens Lisa MBoland GenevieveHerlyn MeenhardMills GordonLiu LunxuZhang Gao - Ferroptosis contributes to acute lung injury (ALI), but whether endogenous oxidized phospholipids trigger epithelial ferroptosis and which intracellular defenses restrain this process remain unclear. We hypothesized that the oxidized phosphatidylcholine POVPC initiates epithelial ferroptosis and that RCN3 functions as a protective intracellular safeguard. - Source: PubMed
Publication date: 2026/03/23
Wang ZhenyanChang JingShi XiaoqianDing FangpingMa Runlin ZWang JingMa YingminJin Jiawei - Although monocyte-to-macrophage differentiation is essential for innate immune defense, its dysregulation can drive excessive inflammation in sepsis. Reticulocalbin 3 (RCN3) is an endoplasmic reticulum chaperone in the secretory pathway implicated in alveolar epithelial maturation and lung injury repair. This study aimed to investigate the effect of RCN3 on monocyte-to-macrophage differentiation in pneumonia-associated sepsis. - Source: PubMed
Publication date: 2026/03/24
Zan DanniXu ZhuoDing FangpingShi XiaoqianChen HongMa YingminJin Jiawei - NSCLC remains one of the leading causes of death from cancer worldwide. Although brain metastases are indeed common and also a significant issue in some cases, what actually causes different patients with NSCLC to develop this condition or not has yet to be clarified by us so as to have a better understanding of the risk. - Source: PubMed
Publication date: 2026/02/26
Zhong LiYanWei XiaoJingJiang JianMing