Ask about this productRelated genes to: MTRR Blocking Peptide
- Gene:
- MTRR NIH gene
- Name:
- 5-methyltetrahydrofolate-homocysteine methyltransferase reductase
- Previous symbol:
- -
- Synonyms:
- cblE
- Chromosome:
- 5p15.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-20
- Date modifiied:
- 2018-07-04
Related products to: MTRR Blocking Peptide
Related articles to: MTRR Blocking Peptide
- Surveillance of Neisseria gonorrhoeae strains, their antimicrobial resistance (AMR) profiles, and transmission dynamics is essential in the prevention and control of gonococcal infections. In Kenya, gonococcal molecular surveillance remains limited, leaving gaps in understanding circulating sequence types (STs). This study characterized Kenyan N. gonorrhoeae isolates using multiple molecular typing schemes. - Source: PubMed
Publication date: 2026/05/19
Kivata Mary WandiaEyase Fredrick LunyagiBulimo Wallace DimbusonOundo ValerieWaguche EstherMbinda Wilton MwemaMbuchi Margaret Wanjiku - - Source: PubMed
Publication date: 2026/05/14
Zhao YouliWang QianHe YanjunWang XiaxiaPan Yunyan - Human methionine synthase (MTR) is an essential enzyme of one carbon metabolism. Consisting of a catalytic N-half and a cobalamin binding C-half, MTR utilises this intricate organometallic cofactor in the methyl transfer from methyltetrahydrofolate to homocysteine producing methionine. Cobalamin loading into MTR, and its subsequent activation, requires methylmalonic aciduria and homocystinuria Type D (MMADHC) protein and methionine synthase reductase (MTRR), respectively. However, the molecular basis of cobalamin binding and activation of human MTR aided by MMADHC and MTRR remains unknown. Here, using cryo-electron microscopy, we determine structures of human MTR in its apo, and cobalamin bound states. Apo MTR adopts a conformation where the two halves of the enzyme act independently with the C-half posed to bind cobalamin. Binding of cobalamin and its activation causes conformational changes in MTR that result in a flexible catalytically active state. AlphaFold predictions, validated by interaction studies, show that MMADHC interacts with the C-half of apo MTR to facilitate cobalamin loading. Unexpectedly we found that MTRR interacts at two distinct sites within the C-half of MTR which may aid in activation. Collectively these findings lay the groundwork to uncover the mechanisms through how MMADHC and MTRR coordinate cobalamin loading and activation of human MTR. - Source: PubMed
Publication date: 2026/05/11
Ferreira Douglas S MMcLennan KatieDiamond CalumVollmar MelanieKiyani WasimFroese D SeanKopec JolaBailey Henry JChalk RodBaslé ArnaudElkins Jonathan MCoker Jesse AYue Wyatt WMcCorvie Thomas J - Stunting remains a major public health concern in Southeast Asia, and is shaped by a complex interplay of genetic, inflammatory, and nutritional factors. This scoping review sought to map genetic polymorphisms associated with stunting in Southeast Asian children and to identify candidate biomarkers for early diagnosis and biologically targeted interventions. Following the Arksey and O'Malley framework and the PCC (Population, Concept, Context) model, a systematic search was conducted across 7 databases. Eligible studies were peer-reviewed, published in English from 2015-2024, involved children under 18 years of age, and investigated gene variants in relation to stunting. A total of 902 records were screened independently by 3 reviewers using predefined criteria, with consensus procedures to resolve any discrepancies. Eleven studies met the final inclusion criteria. Thematic analysis and protein-protein interaction mapping revealed that 5 key polymorphisms-IGF1R, GHSR, MTRR, CASP1, and CARD17-were significant contributors to growth impairment. IGF1R polymorphisms were associated with a 2.46-fold increase in stunting risk (odds ratio [OR], 2.46; 95% confidence interval [CI], 1.60-3.78), while MTRR< variants yielded an OR of 1.93 (95% CI, 1.22-3.05). Similarly, GHSR and CASP1 polymorphisms were linked to increased odds of stunting (OR, 2.15; 95% CI, 1.38-3.34 and OR, 1.67; 95% CI, 1.10-2.54, respectively). These polymorphisms were consistently associated with disrupted growth hormone signaling, chronic inflammation, and nutrient-sensitive pathways. The biological network underlying stunting in this population points to a converging mechanism of impaired endocrine function and inflammatory dysregulation. However, this review's scope is limited by underrepresentation of some Southeast Asian nations and exclusion of non-English literature. Early genetic screening for high-risk biomarkers and precision-driven nutritional interventions may offer more effective strategies to reduce the burden of stunting in Southeast Asian children. - Source: PubMed
Publication date: 2026/04/30
Ismail IsmailNur MuhammadSaini SukmaYakub Alfi Syahar - Lung cancer remains the leading cause of cancer-related deaths worldwide. Despite advances in diagnostics and treatment, most patients are diagnosed at advanced stages. Genetic variants such as single nucleotide polymorphisms (SNPs) may improve early detection and risk prediction. This study investigated the association of PPAR-γ rs1801282 and MTRR rs162036 polymorphisms with non-small cell lung cancer (NSCLC) susceptibility in Egyptians and further evaluated their role through a meta-analysis. - Source: PubMed
Publication date: 2026/05/07
Metwally Yomna FZahran Rasha FEl Sadda Rana RRefaat SherifElsaid Afaf M