FNIP1
- Known as:
- FNIP1
- Catalog number:
- Y213900
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FNIP1
Related genes to: FNIP1
- Gene:
- FNIP1 NIH gene
- Name:
- folliculin interacting protein 1
- Previous symbol:
- -
- Synonyms:
- KIAA1961
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-08-09
- Date modifiied:
- 2016-10-05
Related products to: FNIP1
Related articles to: FNIP1
- B cell development relies on stringent checkpoints that ensure immune competence and eliminate autoreactive clones. Transitional B cells (B220⁺CD93⁺), which emerge from the bone marrow, migrate to the spleen and differentiate into follicular (FO) or marginal zone (MZ) B cells, a process governed by B cell receptor (BCR) signaling strength, metabolic fitness, and survival cues. Here, we identify Folliculin Interacting Protein 1 (Fnip1) as a key regulator of this developmental transition. Using conditional Fnip1-deficient mice ( ), loss of Fnip1 results in a developmental arrest at the transitional B220⁺CD93 stage, severely limiting differentiation into FO and MZ B cells and leading to accumulation of a distinct enlarged CD19 , RAG negative B cells. Fnip1 modulates BCR signaling thresholds and metabolic programming by regulating the AMPK/FLCN/TFEB and CD19/PI3K/Akt/mTORC1 pathways through restricting TFEB access to the nucleus. Using the MD4/mHEL/sHEL tolerance model, we show that Fnip1 is dispensable for negative selection but is essential for maintaining peripheral tolerance. Together, our findings define Fnip1 as a metabolic gatekeeper that integrates nutrient-sensing pathways with BCR signaling to orchestrate transitional B cell fate decisions, promote peripheral tolerance, and maintain immune homeostasis. - Source: PubMed
Publication date: 2026/04/01
Park HeonCulbert RyanSakya DechenSilprasert Raynah RIritani Brian M - : High-grade serous ovarian carcinoma (HGSOC) is notorious for its poor prognosis owing to its inherent biological aggressiveness and development of chemoresistance. The mechanistic target of rapamycin (mTOR) pathway is dysregulated in 55% of epithelial ovarian cancers, representing an appealing therapeutic target. To date, the clinical trials of mTOR inhibitors have shown modest response. In this study, we investigated the mTOR pathway in a clinical cohort of primary, chemo-naive, high-grade ovarian cancer samples, along with its regulatory post-transcriptional miRNA regulation. : We performed differential gene expression analysis on 100 HGSOC patients from TCGA and 80 healthy controls (i.e., normal ovarian tissue) from GTEx. The differentially expressed genes (DEGs) were overlaid onto the KEGG mTOR signalling pathway, followed by functional enrichment analysis. Next, we conducted differential miRNA expression analysis on the same cohort and identified regulatory miRNA-mTOR gene pairs involved in cancer pathogenesis. Finally, we constructed an interaction network and identified key hub genes and miRNAs with potential prognostic significance. : We identified 95 mTOR pathway genes that were significantly differentially expressed, involving upstream regulators, core components, and downstream effectors. Functional pathway analysis revealed a prominent shift toward mTORC1 activation, accompanied by paradoxical activation of autophagy. The let-7 miRNA family was identified as a key regulator of the mTOR pathway, potentially facilitating disease progression. RICTOR downregulation, a key component of the mTORC2 complex, appears to play a critical role in this histotype. In addition, FNIP1, a tumour suppressor gene implicated in mTOR dysregulation, was found to correlate with survival outcomes. : We propose a model of dual activation of mTORC1 and autophagy in HGSOC as the metabolic rewiring enabling cancer progression under nutrient and cellular stress. - Source: PubMed
Publication date: 2026/03/07
Hablase RadwaSisu CristinaKarteris EmmanouilChatterjee Jayanta - Folliculin-interacting protein 1 (FNIP1), a key factor in metabolic regulation networks, has emerged as a focal point in biomedical research. It not only orchestrates energy homeostasis through multiple core signaling pathways but also influences cell fate determination and disease pathogenesis. Although early studies have partially elucidated the mechanisms of FNIP1, whether it can serve as a drug-therapy target for diseases remains inadequately characterized. This review summarizes the recent research progress of FNIP1, focusing on structural determinants that govern its functional plasticity, metabolic pathways modulated by FNIP1-mediated crosstalk, and pathological manifestations resulting from dysregulation of FNIP1. It specifically emphasizes the protein structural basis of FNIP1 as a therapeutic target for diseases such as neurodegenerative diseases, type 2 diabetes, and tumors, as well as the potential for developing FNIP1-related targeted drugs. We aim to construct a conceptual framework for developing precision therapeutic strategies targeting FNIP1-centric regulatory nodes by establishing functional correlations between FNIP1 and other metabolic regulators. - Source: PubMed
Publication date: 2025/11/27
Liang YouxinZhang GuixiaChen XintianGao FeifeiZeng XiaoqvJv YouhuaYe ShicaiZhou Yu - Klebsiella pneumoniae (K. pneumoniae) is one of the pathogens causing clinical mastitis of bovine. Previous studies have demonstrated that mitochondrial damage and dysfunction are important mechanisms of mastitis in dairy cattle. Folliculin interacting protein 1 (FNIP1) is a major metabolic regulator of mitochondrial function with proinflammatory capabilities, but its role in K. pneumoniae-induced mastitis is yet to be elucidated. Thus, the studies were conducted to clarify the role of FNIP1-mediated mitochondrial function in mastitis caused by K. pneumoniae in vivo and in vitro. The experiments verified that K. pneumoniae caused decrease of milk fat and protein synthesis evidently in the mammary glands and bovine mammary epithelial cells (BMECs), accompanied by an imbalance in mitochondrial fission and fusion, increased mitochondrial permeability transition pore opening, decreased membrane potential and ATP content. While the enhancement of mitochondrial function alleviated K. pneumoniae-induced BMECs injury via relieving milk fat and protein dyssynthesis. Notably, transcriptomic analysis revealed that FNIP1 expression was upregulated in BMECs induced by K. pneumoniae. Further investigations revealed FNIP1 silencing improved milk synthesis by alleviating mitochondrial dysfunction caused by K. pneumoniae infection, and further inhibiting the activation of inflammatory factors, which in turn prompted the mammary recovery. In conclusion, K. pneumoniae inhibited mitochondrial function by activating FNIP1, which reducing the synthesis of milk fat and protein, thereby in turn lowers milk quality and induced mastitis. This study showed that FNIP1 has the potential as a novel target for the prevention and control of bovine mastitis. - Source: PubMed
Dong PengfeiYuan ChangningWang ZhihaoMao PengLiu KangjunLi JianjiDong JunshengCui LuyingGuo LongMeng XiaZhu GuoqiangLiu HongyunWang RanZhang LiliWang Heng - Neuroblastoma (NB), a pediatric solid malignancy, is distinguished by hetergenous clinical characteristics, including tumor aggressiveness or spontaneous regression. Nevertheless, the regulatory mechanisms and therapeutic approaches underlying these processes are still mainly unknown. Herein, RAR-related orphan receptor B (RORB) as a transcription factor repressing nuclear factor kappa B (NF-κB) signaling involved in lysosomal biogenesis of NB. RORB attenuated the growth, invasiveness, and metastatic spread of NB cells are identified. From a mechanistic perspective, RORB increased the transcription of nuclear receptor subfamily 1 group D member 1 (NR1D1)- or RIO kinase 3 (RIOK3)- in a circadian clock-dependent manner, resulting in suppression of NF-κB activity, subsequent derepression of folliculin (FLCN)- or folliculin interacting protein 1 (FNIP1)- levels, and decrease of lysosomal biogenesis in NB cells. Meanwhile, in liquid condensates, RNA binding motif protein 10 (RBM10) interacted with RORB to repress its transactivation and exerted oncogenic roles in lysosomal biogenesis and aggressiveness of NB cells. Pre-clinically, a small peptide is able to block the interaction between RBM10 and RORB, and suppresses lysosomal biogenesis, tumorigenesis, and aggressiveness. High levels of RORB, NR1D1, RIOK3, FLCN, and FNIP1, or low expression of RBM10, are linked to favorable prognosis of clinical NB cases. These results indicate that targeting RBM10-repressed RORB activity in liquid condensates inhibits lysosomal biogenesis and NB progression via affecting NF-κB signaling. - Source: PubMed
Publication date: 2025/09/03
Guo YanhuaWang XiaojingYang ChunhuiWang ZhijieWang XiaolinLi XinyueQu JiayingZhou ShunchenZheng LiduanTong Qiangsong