Human Lactamase-Like Protein 2, ᵦ LACTB2
- Known as:
- Human Lactamase-Like Protein 2, ᵦ LACTB2
- Catalog number:
- CG57
- Product Quantity:
- l0
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Human Lactamase-Like Protein 2 ᵦ LACTB2
Related genes to: Human Lactamase-Like Protein 2, ᵦ LACTB2
- Gene:
- LACTB2 NIH gene
- Name:
- lactamase beta 2
- Previous symbol:
- -
- Synonyms:
- CGI-83
- Chromosome:
- 8q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-09
- Date modifiied:
- 2015-11-23
Related products to: Human Lactamase-Like Protein 2, ᵦ LACTB2
Related articles to: Human Lactamase-Like Protein 2, ᵦ LACTB2
- Mammalian postnatal life requires adaptation to a carbohydrate-rich diet, yet how metabolic programs are coordinated within and across organs is unclear. Using time-resolved transcriptomic and metabolomic analyses from the neonatal period through adulthood, we show that mouse liver rapidly acquires oxidative and detoxification capacity after weaning. This transition enables the brain to establish energy-sufficient, low-toxicity metabolic environment for neuronal function. This maturation process is marked by progressive activation of the hepatic electron transport chain (ETC), with the mitochondrial RNA endoribonuclease LACTB2 acting as a key regulator. LACTB2 prevents the accumulation of mitochondrial RNAs and sustains expression of mtDNA-encoded ETC subunits, thereby preserving mitochondrial competence for oxidative metabolism. LACTB2 is postnatally induced in hepatocytes, and its loss causes defective glucose utilization, systemic metabolic toxicity, and impaired brain metabolism and myelination, leading to prepubertal lethality, particularly in males. Restoring ETC function through liver-targeted expression of yeast NADH dehydrogenase NDI1, inhibiting the integrated stress response or ammonia scavenging improved survival. Our findings identify LACTB2-dependent hepatic mitochondrial maturation as a central mechanism that aligns carbohydrate adaptation with the liver-brain metabolic coordination to support early-life development. - Source: PubMed
Publication date: 2025/11/06
Cui HongmeiWu ZhengZhang YuannyuVu Hieu SChen HongliGao XiaofeiJin YanCai DonghongAchyutuni SaradaNguyen PhongPan ChunxiaoCao HuiRobinson Camenzind GSteinberg Jeffery DJanke Laura JNowinski Sara MXu JianDeBerardinis Ralph JNi Min - Mitochondrial dysfunction is increasingly recognized as a key factor in neurodegenerative diseases (NDDs), underscoring the therapeutic potential of targeting mitochondria-related genes. This study aimed to identify novel biomarkers and drug targets for these diseases through a comprehensive analysis that integrated genome-wide Mendelian randomization (MR) with genes associated with mitochondrial function. - Source: PubMed
Publication date: 2025/01/22
Wang ZheyiSun YizeBai ZetaiLi MeiKong DeyuanWu Guanzhao - This study aims to identify m6A methylation-related and immune cell-related key genes with diagnostic potential for heart failure (HF) by leveraging various bioinformatics techniques. - Source: PubMed
Publication date: 2024/10/16
Wu ZelanLiu WupengSi XiaoyunLiang Jinfeng - The pregnant women with intrahepatic cholestasis were at high risk of fetal distress, preterm birth and unexpected stillbirth. Intrahepatic cholestasis of pregnancy (ICP) was mainly caused by disorder of bile acid metabolism, whereas the specific mechanism was obscure. - Source: PubMed
Publication date: 2024/08/10
Fang YanKang ZheZhang WeiqiangXiang YunCheng XiGui MianFang Dajun - This study aimed to investigate the mechanisms of LACTB2 in colorectal cancer (CRC). Microarrays and sequencing data of CRC were acquired from UCSC Xena, GTEx, Gene Expression Omnibus, and TCGA. Pooled analysis of the mRNA expression of LACTB2 in CRC was performed using Stata software. The protein expression of LACTB2 in CRC tissues was evaluated by immunohistochemistry. The relationship between immune cell infiltration and LACTB2 expression was investigated using CIBERSORT. The potential signaling pathways and biological mechanisms of LACTB2 were explored using GSEA, KEGG, and GO. Subsequently, further screening of small molecular compounds with potential therapeutic effects on CRC was conducted through the HERB database, followed by molecular docking studies of these compounds with the LACTB2 protein. The integration and analysis of expression data obtained from 2294 CRC samples and 1286 noncancerous colorectal samples showed that LACTB2 was highly expressed in CRC. Immunohistochemistry performed on in-house tissue samples confirmed that LACTB2 protein expression was upregulated in CRC. CIBERSORT revealed lower B cell infiltration levels in the high LACTB2 expression group than in the low expression group. GO, KEGG, and GSEA analyses showed that LACTB2 expression and genes positively correlating with it were mainly related to DNA synthesis and repair, mitochondrial translational elongation and translational termination, phosphorylation, and mTORC1 signaling. Finally, molecular docking simulations confirmed the ability of quercitin to target and bind to LACTB2. This is the first study to demonstrate that LACTB2 is upregulated in CRC. LACTB2 promotes colorectal tumorigenesis and tumor progression. - Source: PubMed
Publication date: 2024/04/25
Li HuiWen Jia-YingLiu Cui-ZhenFang Ye-YingYe Yu-PingZeng Da-TongPan Yan-FangChen Zu-XuanLiu Li-MinSong Rui