Ask about this productRelated genes to: MAT2B Blocking Peptide
- Gene:
- MAT2B NIH gene
- Name:
- methionine adenosyltransferase 2B
- Previous symbol:
- -
- Synonyms:
- MATIIbeta, SDR23E1
- Chromosome:
- 5q34
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-01
- Date modifiied:
- 2016-01-27
Related products to: MAT2B Blocking Peptide
Related articles to: MAT2B Blocking Peptide
- Sepsis caused by carbapenem-resistant Klebsiella pneumoniae (CRKP) is associated with high mortality. Current research is predominantly pathogen-centric, creating a knowledge gap regarding the host's systemic molecular response, which is critical for understanding outcomes and developing diagnostic strategies. This study aimed to characterize the host serum proteomic and metabolomic landscape of CRKP sepsis and to develop a proteomics-derived biomarker panel for differential diagnosis, while integrating metabolomic data to gain mechanistic insights into host pathways. - Source: PubMed
Publication date: 2026/05/20
He JuanLuo SiqiXu WenyunChen YuanzhuoLiu GuorongTang JianguoYang YongZhao BingMa LiSheng HuiqiuMao Enqiang - Lung adenocarcinoma (LUAD) is a highly heterogeneous malignancy with poor clinical outcomes, underscoring the urgent need for robust prognostic biomarkers and therapeutically tractable regulatory molecules. Long non-coding RNAs (lncRNAs) have emerged as key modulators of tumor progression and immune regulation; however, the prognostic and functional significance of TMPO-AS1 in LUAD remains largely unexplored. - Source: PubMed
Publication date: 2026/04/13
Nirmal SakshiSaini ChainseeBaweja BhavikaVats PrernaPatidar PrachiJangir KritikaNema Rajeev - ARF GTPase protein 1 (GIT1) is a scaffold protein that is overexpressed in hepatocellular carcinoma (HCC) and colorectal cancer (CRC). GIT1 forms a complex with methionine adenosyltransferase 2B (MAT2B) that activates RAS-RAF-MEK-ERK signaling in HCC and CRC to enhance tumorigenicity. Here, we investigated in a proof-of-concept study whether a small molecule that disrupts GIT1-MAT2B interaction can be effective in HCC and CRC treatment. Since the GIT1 crystal structure is unavailable, we developed a molecular model and used computer-based drug discovery approach to screen for small molecules targeting the GIT1 ankyrin repeat domain, the region closest to where MAT2B interacts that is accessible. Of nine compounds tested, compound 3 (C3) selectively interacts with GIT1 and shows an anti-cancer effect in a GIT1-dependent manner. C3 is antiproliferative, induced apoptosis and G2/M cell cycle arrest while inhibiting colony formation and migration in liver and colon cancer cells. C3 lowered interaction between GIT1 and MAT2B, and with downstream effectors cRAF, MEK and ERK, lowering MEK activity and cyclin D1 expression. Unexpectedly, C3 stabilized GIT1 interaction with cyclin B1 while weakening cyclin B1's interaction with components of the anaphase promoting complex, concomitant with sustained cyclin B1 expression and mitosis arrest. In mice, C3 administration was well tolerated and inhibited murine CRC growth and liver metastasis in immune competent mice and human CRC growth in the livers of nude mice. In conclusion, a small molecule inhibitor that disrupts GIT1's normal interactome is a promising new approach to treating liver and colon cancers. - Source: PubMed
Publication date: 2026/02/20
Peng HuiChhimwal JyotiFan WeiWang JiaohongBarbier-Torres LucíaSinha SonalChatterjee AvradipZhang YiTomasi Maria LaudaMato José MMurali RamachandranLu Shelly C - Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), an oncofetal RNA-binding protein and a non-canonical reader of N6-methyladenosine (mA) mRNA modifications, is known to be critical for leukemogenesis. To understand how the oncogenic function of IGF2BP3 impacts metabolism, we performed metabolic profiling and observed changes in glycolytic flux and one-carbon metabolism, including the biosynthesis of S-adenosyl methionine (SAM), a key substrate for methylation reactions within the cell. Using enhanced crosslinking immunoprecipitation (eCLIP) and polyribosome profiling, we found that IGF2BP3 promotes translation of the regulatory subunit of the methionine adenosyltransferase complex (MAT2B), which is involved in SAM production. Remarkably, IGF2BP3 promotes and alters the level and pattern of mA modifications on mRNA. Taken together, these data suggest the intriguing hypothesis that IGF2BP3 rewrites the epitranscriptome in leukemia cells. Furthermore, this work highlights an interconnection between oncogenic metabolism and RNA modifications, suggesting that pervasive gene expression changes necessary for oncogenesis may be perpetuated by post-transcriptional gene regulation. - Source: PubMed
Publication date: 2025/09/26
Sharma GunjanGutierrez MartinJones Anthony EKapoor ShrutiJaiswal Amit KumarNeeb Zachary TRios AmyDorairaj PoornimaThaxton Michelle LLin Tasha LTran Tiffany MKabbani Lyna E SRitter Alexander JScherer Georgia MSorrentino Jacob PStiles LinseyHoeve Johanna TenDamoiseaux Robert DGarg Neil KDivakaruni Ajit SSanford Jeremy RRao Dinesh S - Astrocytes play a critical role in maintaining the integrity of the blood-brain barrier (BBB) under physiological conditions and become activated and secrete certain inflammatory cytokines under inflammatory conditions. These inflammatory factors directly or indirectly exacerbate BBB disruption by regulating the expression of tight junction proteins (TJPs), which are located between brain capillary endothelial cells. It has been reported that the protective function of the BBB, which is fundamental for homeostasis and normal neuronal activity, could be altered during stress conditions. MiR-142 is one of the most abundant miRNAs in the brain and is considered a molecular link between inflammation and neuronal dysfunction. The present research focused on studying the impact of microRNA-142 (miR-142)-5p on the regulation between astrocytes and brain microvascular endothelial cells (BMVECs) under a simulated inflammatory condition. The results of the present study showed that the miR-142 inhibition could alleviate the disruption of BMVECs induced by lipopolysaccharide (LPS) induced astrocytic media (L-ACM) through upregulating the expression of tight junction proteins (TJPs), increasing the ratio of Bcl-2/Bax and downregulating the level of NF-κB. This effect of miR-142-5p inhibition might complement through binding to Methionine adenosyltransferase 2B (MAT2B). Taken together, the downregulation on the miR-142-5p level in BMVECs might be a promising therapeutic strategy for BBB damage in inflammatory condition. - Source: PubMed
Publication date: 2025/06/09
Liu Chun-YuChen Dun-ChaoZhang Zi-HangLi Tai-RanJi Li-Li