Ask about this productRelated genes to: FAM83F antibody
- Gene:
- FAM83F NIH gene
- Name:
- family with sequence similarity 83 member F
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-27
- Date modifiied:
- 2019-02-20
Related products to: FAM83F antibody
Related articles to: FAM83F antibody
- The present study aimed to explore runs of homozygosity (ROH), Heterozygosity Enriched Regions (HER) using the sliding window approach in both PLINK and detectRUNS, as well as the consecutive SNP approach in detectRUNS and their association with important economic traits. Genomic inbreeding coefficient based on ROH and heterosis coefficient based on HER were also estimated among crossbred (n = 81) by using GGP_HDv3_C genotyping assay. Total ROH varied from around 600 in the sliding window approach and almost double in the Consecutive SNP approach of detectRUNS. Similarly, the HER are 756 in the sliding window and 771 in the Consecutive SNP method. The mean inbreeding coefficient range varied in different approaches, i.e., 0.016-0.022 is observed based on ROH (Froh), and the heterosis coefficient based on HER (Frohet) is 0.0019. Top ROH and HER regions contain important genes related to dairy (EHHADH, CACNA1C, MICALL1, EIF3L, GTPBP1, SYNGR1, ATF4, GRAP2, FAM83F, ACO2), immunity (LIPH, TMEM41A, PEX26, CDC42EPI, CXXC5, PSD2, PURA, CYSTM1, RNF14), growth and carcass (MAGEF1, TGS1, LYN, CHCHD7, FAM110B, SDCBP, SH3BP1, GGA1, TRIOBP, PICK1, MAFF, TOMM22, MGAT3, TNRC6B, ADSL, EP300, SMDT1, MATR3) traits. These findings may provide valuable insights into the understanding of genome-wide homozygosity and heterozygosity patterns and genetic architecture of the Pakistani crossbred cattle. - Source: PubMed
Publication date: 2025/09/26
Nisa Fakhar UnUsman MuhammadAli AsadAli Muhammad BasilKaul HaibaAsif MuhammadMrode RaphaelMukhtar Zahid - Cancer-associated fibroblasts (CAFs) have been shown to play a crucial role in the progression of non-small cell lung cancer (NSCLC). Exosomes derived from CAFs have emerged as important mediators of intercellular communication in the tumor microenvironment, contributing to cancer progression. Therefore, it is essential to further investigate the mechanisms by which CAF-derived exosomes regulate NSCLC. CAFs promoted NSCLC cell proliferation, invasion, and migration, while also suppressing radiosensitivity. We observed an upregulation of FAM83F expression in both NSCLC cells and NSCLC cells treated with conditioned medium from CAFs. Notably, CAF-derived exosomes were found to transfer FAM83F to NSCLC cells, thereby enhancing the malignant properties of the cancer cells. In contrast, FAM83F-deficient CAF-derived exosomes exerted inhibitory effects on NSCLC cell proliferation, invasion, and migration, while also sensitizing the cells to radiotherapy. FAM83F was found to interact with KIF23 in NSCLC cells, and the overexpression of KIF23 attenuated the effects induced by FAM83F-deficient exosomes in NSCLC cells. Moreover, FAM83F-deficient CAF-derived exosomes were effective in inhibiting tumor formation . Our findings highlight the crucial role of CAF-derived exosomal FAM83F in promoting NSCLC progression and conferring resistance to radiotherapy. Targeting this signaling pathway may offer promising therapeutic strategies for combating NSCLC progression and improving patient outcomes. - Source: PubMed
Publication date: 2025/01/25
Li YiZhou MingmingHu XiaogangXie TingtingPeng WenliZhang LinaTang MinxinHu RuiHe Yongpeng - Reports of traditional Chinese medicine (TCM)-related liver injury have increased over recent years; however, identifying susceptibility-related components and biomarkers remains challenging due to the heterogeneous nature of TCM and idiosyncratic drug-induced liver injury (IDILI). (PF) and (EF), commonly found in TCM prescriptions, have been implicated in IDILI, but their constituents and underlying mechanisms are poorly understood. In this study, we identified bavachin (Bav) and icariin (Ica) as susceptibility components for IDILI in PF and EF using a TNF-α-mediated mouse model. Lipidomics and transcriptomics were used to investigate their related mechanism. Liver biochemistry and histopathology analyses revealed that co-exposure to Bav, Ica, and a non-toxic dose of TNF-α prestimulation induced significant liver injury, while Bav and Ica alone did not. Lipidomics identified seven differentially abundant metabolites in the Bav/Ica/TNF-α group compared to the Ica/TNF-α or Bav/TNF-α groups, mainly enriched in alpha-linolenic acid (ALA), arachidonic acid (AA), and linoleic acid (LA) metabolic pathways. Additionally, transcriptomics revealed 49 differentially expressed genes (DEGs) in the Bav/TNF-α vs Bav/Ica/TNF-α and Ica/TNF-α vs Bav/Ica/TNF-α groups, primarily associated with the PI3K/AKT/mTOR signaling pathway and sphingolipid metabolism. Integrative lipidomics and transcriptomics analyses identified significant positive correlations between five differential metabolites (DMs) - PC (O-16:0_14:1), PG (22:1_20:3), PI (16:0_14:1), PS (18:0_19:2), and TG (17:0_18:2_22:5) - and ten DEGs - . Collectively, these results suggest that alterations in intracellular metabolism and gene expression levels may contribute to the synergistic induction of IDILI by the incompatible pair Bav and Ica in the presence of TNF-α. - Source: PubMed
Publication date: 2024/11/06
Li YingyingCao BoLin MengmengXu JingQi ShuyaWang JiaboXiao XiaoheLi GuohuiLi Chunyu - The FAM83 (ily with sequence similarity ) family is highly conserved in vertebrates, but little is known of the functions of these proteins beyond their association with oncogenesis. Of the family, FAM83F is of particular interest because it is the only membrane-targeted FAM83 protein. When overexpressed, FAM83F activates the canonical Wnt signalling pathway and binds to and stabilizes p53; it therefore interacts with two pathways often dysregulated in disease. Insights into gene function can often be gained by studying the roles they play during development, and here we report the generation of knock-out (KO) zebrafish, which we have used to study the role of Fam83f . We show that endogenous is most strongly expressed in the hatching gland of developing zebrafish embryos, and that KO embryos hatch earlier than their wild-type (WT) counterparts, despite developing at a comparable rate. We also demonstrate that KO embryos are more sensitive to ionizing radiation than WT embryos-an unexpected finding, bearing in mind the previously reported ability of FAM83F to stabilize p53. Transcriptomic analysis shows that loss of leads to downregulation of phosphatidylinositol-3-phosphate (PI(3)P) binding proteins and impairment of cellular degradation pathways, particularly autophagy, a crucial component of the DNA damage response. Finally, we show that Fam83f protein is itself targeted to the lysosome when overexpressed in HEK293T cells, and that this localization is dependent upon a C' terminal signal sequence. The zebrafish lines we have generated suggest that Fam83f plays an important role in autophagic/lysosomal processes, resulting in dysregulated hatching and increased sensitivity to genotoxic stress . - Source: PubMed
Publication date: 2024/10/23
Jones Rebecca ACooper FayKelly GavinBarry DavidRenshaw Matthew JSapkota GopalSmith James C - Cervical cancer (CC) seriously affects women's health. Therefore, elucidation of the exact mechanisms and identification of novel therapeutic targets are urgently needed. In this study, we identified FAM83F, which was highly expressed in CC cells and tissues, as a potential target. Our clinical data revealed that FAM83F protein expression was markedly elevated in CC tissues and was positively correlated with poor prognosis. Moreover, we observed that FAM83F knockdown significantly inhibited cell proliferation, induced apoptosis, and suppressed glycolysis in CC cells, while its overexpression displayed opposite effects. Mechanistically, FAM83F regulated CC cell growth and glycolysis by the modulation of Wnt/β-catenin pathway. The enhancing effects of FAM83F overexpression on CC cell proliferation and glycolysis could be impaired by the Wnt/β-catenin inhibitor XAV939. Moreover, we found that c-Myc bound to the FAM83F promoter and activated the transcription of FAM83F. Notably, knockdown of FAM83F impaired the enhancement of cell proliferation and glycolysis induced by ectopic c-Myc. Consistent with in vitro findings, results from a xenograft mouse model confirmed the promoting role of FAM83F. In summary, our study demonstrated that FAM83F promoted CC growth and glycolysis through regulating the Wnt/β-catenin pathway, suggesting that FAM83F may be a potential molecular target for CC treatment. Schematic summary of c-Myc-activated FAM83F transcription to promote cervical cancer growth and glycolysis by targeting the Wnt/β-catenin signal pathway. - Source: PubMed
Publication date: 2023/12/16
Zhang ChanglinLiu LixiangLi WeizhaoLi MengxiongZhang XunzhiZhang ChiYang HuanXie JiayuanPan WeiGuo XueShe PengZhong LiLi Tian