C6orf168
- Known as:
- C6orf168
- Catalog number:
- 003208A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- C6orf168
Related genes to: C6orf168
- Gene:
- FAXC NIH gene
- Name:
- failed axon connections homolog, metaxin like GST domain containing
- Previous symbol:
- C6orf168
- Synonyms:
- MGC2817, dJ273F20
- Chromosome:
- 6q16.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-16
- Date modifiied:
- 2019-01-14
Related products to: C6orf168
Related articles to: C6orf168
- Renal cell carcinoma (RCC), the most common types of kidney cancer, still requires novel therapeutic targets to improve patients' outcome. In this study, we focus on Failed Axon Connections Homolog (FAXC) gene, a newly identified and potentially important cancer target, and investigated its detailed role in RCC. In RCC cells, FAXC knockdown resulted in increased cell proliferation, and elevated c-MET expression and phosphorylation. Blockade of c-MET phosphorylation inhibited cell proliferation promoted by FAXC knockdown. In contrast, FAXC overexpression reduced cell proliferation and downregulated c-MET expression in RCC cells. We also found that FAXC is localized to the mitochondria in RCC cells. Additionally, an investigation of RCC patient specimens revealed that FAXC expression was negatively correlated with c-MET phosphorylation and was downregulated in tumor region compared with adjacent normal tissues. Taken together, our findings indicate that FAXC depletion promotes cell proliferation through the activation of c-MET in RCC cells. - Source: PubMed
Publication date: 2025/07/18
Konno MasatoFujimori HarunaKanno Shin-IchiroShibuya-Takahashi RieMochizuki MaiYamaguchi KazunoriYasuda JunMurakami ShigekazuSatoh KennichiAdachi HisanobuIto AkihiroTamai KeiichiAsano Naoki - A detailed understanding of the precise regulatory mechanisms governing buffalo skeletal muscle is crucial for improving meat quality and yield. Proper skeletal muscle fate decisions necessitate the accurate regulation of key enhancers. This study screened nine potential enhancers linked to muscle development by analysing ATAC-seq data from buffalo myoblasts during the proliferative and differentiative phases. The enhancer activity of these candidates was confirmed in buffalo myoblasts, C2C12, and human skeletal muscle myoblasts using a dual-luciferase reporter system. The CRISPRi system and RT-qPCR were used to test the effects of 9 candidate enhancers on buffalo myoblasts. The active enhancer, Enh483, was selected based on its significant impact. Upon successful inhibition of Enh483 using CRISPRi, decreases in the expression of buffalo myogenic proliferation marker genes (PCNA, CyclinD1, and CDK2) were observed via RT-qPCR and Western blot. Subsequent proliferation assays using CCK-8 and EdU confirmed the promotive effect of Enh483 on buffalo myogenic cell proliferation. Following a 5-day differentiation induction period, changes in the expression of differentiation marker genes (MyoD1, MyoG, and MyHC) were analysed using RT-qPCR and Western blot. Additionally, fused myotube numbers were quantified, and the impact of Enh483 on buffalo myogenic cell differentiation was assessed through immunofluorescence. Our findings indicate that Enh483 facilitates buffalo myogenic cell differentiation. Further interaction analysis utilising 3C-PCR revealed a direct association between Enh483 and the FAXC promoter. In summary, the results from this study lay a foundational framework for deciphering the intricate regulatory mechanisms underpinning buffalo muscle development. - Source: PubMed
Publication date: 2024/12/17
Chen YalingZhao JiahuiZhong CuiweiKang YujinXiong ZhaochengHuang JiepingLi ZhipengLiu QingyouShi DeshunLi XinxinWang JianLi Hui - Cholangiocarcinoma (CCA) is one of the most difficult malignancies to treat as the therapeutic options are limited. Although several driver genes have been identified, most remain unknown. In this study, we identified a failed axon connection homolog (FAXC), whose function is unknown in mammals, by analyzing serially passaged CCA xenograft models. Knockdown of FAXC reduced subcutaneous tumorigenicity in mice. FAXC was bound to annexin A2 (ANXA2) and c-SRC, which are tumor-promoting genes. The FAXC/ANXA2/c-SRC complex forms in the mitochondria. FAXC enhances SRC-dependent ANXA2 phosphorylation at tyrosine-24, and the C-terminal amino acid residues (351-375) of FAXC are required for ANXA2 phosphorylation. Transcriptome data from a xenografted CCA cell line revealed that FAXC correlated with epithelial-mesenchymal transition, hypoxia, and KRAS signaling genes. Collectively, these findings advance our understanding of CCA tumorigenesis and provide candidate therapeutic targets. - Source: PubMed
Publication date: 2024/03/13
Fujimori HarunaShima-Nakamura MaoKanno Shin-IchiroShibuya-Takahashi RieMochizuki MaiMizuma MasamichiUnno MichiakiWakui YutaAbue MakotoIwai WataruFukushi DaisukeSatoh KennichYamaguchi KazunoriShindo NorihisaYasuda JunTamai Keiichi - There is only one report of patients with developmental delay due to a 6q16.1 deletion that does not contain the SIM1 gene. A 3-year-old female showed strabismus, cleft soft palate, hypotonia at birth, and global developmental delay. Exome sequencing detected a de novo 6q16.1 deletion (chr6: 99282717-100062596) (hg19). The following genes were included in this region: POU3F2, FBXL4, FAXC, COQ3, PNISR, USP45, TSTD3, CCNC, and PRDM13. - Source: PubMed
Publication date: 2022/05/17
Okazaki TetsuyaKawaguchi TatsuyaSaiki YusukeAoki ChisakoKasagi NorikoAdachi KaoriSaida KenMatsumoto NaomichiNanba EijiMaegaki Yoshihiro