FAM80A Blocking Peptide
- Known as:
- FAM80A Blocking Peptide
- Catalog number:
- 33r-2255
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- FAM80A Blocking Peptide
Related genes to: FAM80A Blocking Peptide
- Gene:
- RIMKLA NIH gene
- Name:
- ribosomal modification protein rimK like family member A
- Previous symbol:
- FAM80A
- Synonyms:
- MGC47816, RP11-157D18.1, NAAGS-II
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-21
- Date modifiied:
- 2018-03-15
Related products to: FAM80A Blocking Peptide
Related articles to: FAM80A Blocking Peptide
- The increasing incidence and mortality of thyroid cancer (THCA) exacerbates the global cancer burden. Glutamine metabolism is a hallmark metabolic feature of tumors, but its impact on the pathogenesis and progression of THCA remains unclear. Studies retrieved THCA data from TCGA and GEO databases. Cluster analysis, differential expression analysis, and weighted gene co-expression network analysis were used to identify key glutamine metabolism-related genes (GMRGs) in THCA. Identification of key genes through protein-protein interaction network construction, based on expression and diagnosis of internal and external datasets. Their functional role was systematically evaluated by competitive endogenous RNA network analysis, genomic alteration analysis, immune-related studies, and immune checkpoint analysis. Using GMRGs and differentially expressed genes in THCA, 6 markers (NOS2, OTC, NOS1, GLS2, UCP2, RIMKLA) were selected as references for THCA clustering. Differential analysis combined with weighted gene co-expression network analysis identified 173 GMRGs in THCA. The CytoHubba algorithm in the protein-protein interaction network identified 4 hub genes: MUC1, KIT, COMP, and MMP7. Subsequent validation showed a significant decrease in the expression of KIT in tumor samples (P < .05). Receiver operating characteristic curve (ROC) analysis showed excellent diagnostic performance with area under the curve values of 0.925, 0.945, 0.965, and 0.996 in the internal and external validation cohorts. Notably, KIT expression showed a significant difference between T and N phases (P < .05). In addition, we delineate a regulatory network of competitive endogenous RNAs that control KIT expression. Genomic alteration analysis reveals frequent KIT modifications in anaplastic thyroid carcinoma. Tumors with low KIT expression exhibited enhanced immune infiltration and significant correlation with immune checkpoint genes, including PDCD1LG2 and PDCD1 (P < .05). This study identifies KIT as a key GMRG in THCA, positioning it as a novel diagnostic biomarker and a potential therapeutic evaluation marker for tumor progression. - Source: PubMed
Li XinxiongQiu LizhenGu EnyuKe NaizhuoFang Miao - Breast cancer is a complex and multifaceted disease with diverse risk factors, types, and treatment options. Triple-negative breast cancer (TNBC), which lacks the expression of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2), is the most aggressive subtype. Hypoxia is a common feature of tumors and is associated with poor prognosis. Hypoxia can promote tumor growth, invasion, and metastasis by stimulating the production of growth factors, inducing angiogenesis, and suppressing antitumor immune responses. In this study, we used mRNA-seq technology to systematically investigate the gene expression profile of MDA-MB-231 cells under hypoxia. We found that the hypoxia-inducible factor (HIF) signaling pathway is the primary pathway involved in the cellular response to hypoxia. The genes in which expression levels were upregulated in response to hypoxia were regulated mainly by HIF1α. In addition, hypoxia upregulated various genes, including , , , , , , and , suggesting that it regulates cellular processes beyond angiogenesis, metabolism, and known processes. We also found that HIF1α was hyperactivated in MDA-MB-231 cells under normoxia. A HIF1α inhibitor effectively inhibited the invasion, migration, proliferation, and metabolism of MDA-MB-231 cells. Our findings suggest that hypoxia and the HIF signaling pathway play more complex and multifaceted roles in TNBC than previously thought. These findings have important implications for the development of new therapeutic strategies for TNBC. - Source: PubMed
Publication date: 2024/07/31
Han DelongLi ZeyuLuo LingjieJiang Hezhong - Nonalcoholic fatty liver disease (NAFLD) is a serious threat to public health, but its underlying mechanism remains poorly understood. In screening important genes using Gene Importance Calculator (GIC) we developed previously, ribosomal modification protein rimK-like family member A (RIMKLA) was predicted as one essential gene but its functions remained largely unknown. The current study determined the roles of RIMKLA in regulating glucose and lipid metabolism. RIMKLA expression was reduced in livers of human and mouse with NAFLD. Hepatic RIMKLA overexpression ameliorated steatosis and hyperglycemia in obese mice. Hepatocyte-specific RIMKLA knockout aggravated high-fat diet (HFD)-induced dysregulated glucose/lipid metabolism in mice. Mechanistically, RIMKLA is a new protein kinase that phosphorylates betaine-homocysteine S-methyltransferase 1 (BHMT1) at threonine 45 (Thr45) site. Upon phosphorylation at Thr45 and activation, BHMT1 eliminated homocysteine (Hcy) to inhibit the activity of transcription factor activator protein 1 (AP1) and its induction on fatty acid synthase (FASn) and cluster of differentiation 36 (CD36) gene transcriptions, concurrently repressing lipid synthesis and uptake in hepatocytes. Thr45 to alanine (T45A) mutation inactivated BHMT1 to abolish RIMKLA's repression on Hcy level, AP1 activity, FASn/CD36 expressions, and lipid deposition. BHMT1 overexpression rescued the dysregulated lipid metabolism in RIMKLA-deficient hepatocytes. In summary, RIMKLA is a novel protein kinase that phosphorylates BHMT1 at Thr45 to repress lipid synthesis and uptake. Under obese condition, inhibition of RIMKLA impairs BHMT1 activity to promote hepatic lipid deposition. - Source: PubMed
Publication date: 2024/08/08
Yan HanLiu WenjunXiang RuiLi XinHou SongXu LuzhengWang LinZhao DongLiu XingkaiWang GuoqingChi YujingYang Jichun - Diabetic foot ulcer (DFU) is one of the most common and severe complications of diabetes, with vascular changes, neuropathy, and infections being the primary pathological mechanisms. Glutamine (Gln) metabolism has been found to play a crucial role in diabetes complications. This study aims to identify and validate potential Gln metabolism biomarkers associated with DFU through bioinformatics and machine learning analysis. - Source: PubMed
Publication date: 2024/01/30
Shi HongshuoYuan XinYang XiaoHuang RenyanFan WeijingLiu Guobin - Canavan disease (CD) is a leukodystrophy caused by mutations in the N-acetylaspartate (NAA) hydrolase aspartoacylase (ASPA). Inability to degrade NAA and its accumulation in the brain results in spongiform myelin degeneration. NAA is mainly synthesized by neurons, where it is also a precursor of the neuropeptide N-acetylaspartylglutamate (NAAG). Hydrolysis of this peptide by glutamate carboxypeptidases is an additional source of extracellular NAA besides the instant neuronal release of NAA. This study examines to what extent NAA released from NAAG contributes to NAA accumulation and pathogenesis in the brain of Aspa mutant mice, an established model of CD. Towards this aim, Aspa mice with additional deficiencies in NAAG synthetase genes Rimklb and/or Rimkla were generated. Loss of myelin in Aspa mice was not significantly affected by Rimkla and Rimklb deficiency and there was also no obvious change in the extent of brain vacuolation. Astrogliosis was slightly reduced in the forebrain of Rimkla and Rimklb double deficient Aspa mice. However, only minor improvements at the behavioral level were found. The brain NAA accumulation in CD mice was, however, not significantly reduced in the absence of NAAG synthesis. In summary, there was only a weak tendency towards reduced pathogenic symptoms in Aspa mice deficient in NAAG synthesis. Therefore, we conclude that NAAG metabolism has little influence on NAA accumulation in Aspa mice and development of pathological symptoms in CD. - Source: PubMed
Publication date: 2023/11/27
Becker IvonneWang-Eckhardt LihuaEckhardt Matthias