Ask about this productRelated genes to: TCN2 antibody
- Gene:
- TCN2 NIH gene
- Name:
- transcobalamin 2
- Previous symbol:
- -
- Synonyms:
- D22S676, D22S750, TC2
- Chromosome:
- 22q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: TCN2 antibody
Related articles to: TCN2 antibody
- Normal pregnancy involves modulation of thousands of maternal plasma proteins, and departures from the normal trajectories may be indicative of the development of adverse pregnancy outcomes. A decrease in placental growth factor (PlGF) and an increase in soluble fms-like tyrosine kinase 1 (sFlt-1) in maternal plasma were shown to be associated with fetal death at the time of diagnosis and to predict this devastating pregnancy outcome at 24-28 weeks of gestation. However, these proteomic dysregulations are also present in other obstetrical syndromes, and more specific and sensitive biomarkers are needed to implement preventive strategies. - Source: PubMed
Publication date: 2026/04/02
Romero RobertoBhatti GauravChaiworapongsa TinnakornGomez-Lopez NardhyMeyyazhagan ArunChaemsaithong PiyaJung EunjungAwonuga Awoniyi OKim Yeon MeeGudicha Dereje WJai Kim ChongBryant David RHassan Sonia STarca Adi L - In two large, ethnically different prospective cohorts from the UK and Hong Kong, osteoporosis was associated with a higher risk of age-related cataracts, particularly in women. Proteomic mediation analysis identified five circulating proteins (MEPE, GDF15, TCN2, CDCP1, SIGLEC1) that may link osteoporosis to cataract development, warranting future mechanistic investigation. - Source: PubMed
Publication date: 2026/02/24
Zhang XiaowenKrishnamoorthy SuhasChong Kelvin K LMak Jonathan K LTan Kathryn Choon-BengKung Annie Wai-CheeWong Ian Chi-KeiZheng Hou-FengCheung Ching-Lung - Emerging evidence suggests that chronic use of gastric acid-suppressing medications may contribute to neurocognitive decline, yet the underlying mechanisms remain poorly defined. Proton pump inhibitors like omeprazole and histamine-2 receptor antagonists such as ranitidine are widely prescribed for gastrointestinal disorders, but their long-term impact on brain function. Forty-eight male Wistar rats were assigned to six groups receiving either control diet, B alone, omeprazole, ranitidine, or co-treatment with B for 90 days. Behavioral and cognitive assessments revealed early deficits in the drug-only-treated groups (omeprazole and ranitidine). Notably, B ameliorated omeprazole-induced impairments but failed to reverse ranitidine-associated deficits, suggesting divergent neurotoxic pathways. Biochemical profiling included serum B, homocysteine, cortisol, glucose, insulin, liver enzymes, and neurotransmitter. To complement these in vivo findings, an in silico approach was employed to explore molecular interactions of omeprazole and ranitidine with proteins critical for vitamin B transport (CBLIF and TCN2) and cholinergic neurotransmission (CHRNA7). Together, these in vivo and in silico results suggest that omeprazole-induced cognitive decline may involve B depletion and other mechanisms, whereas ranitidine likely acts via alternative pathways. This study provides novel mechanistic insights into differential cognitive risks associated with chronic acid-suppressing therapy, with implications for long-term management in populations vulnerable to neurodegeneration. - Source: PubMed
Saihati Hajir A AlAhmed Bushra YMosaad Rehab MEl-Garhy Hoda A SBakeer Rofanda MYousef Einas MAhmed Inas MNasr Walaa S Saif ElShadi-Dizaji AzizehAhmed-Farid Omar AWarda Mohamad - Hypoxia is a hallmark of the tumor microenvironment that profoundly alters the cellular metabolism and epigenetic regulation. In this study, we investigated how oxygen limitation reprograms histone methylation in glioblastoma cells by integrating stable isotope tracing with high-resolution proteomics and epigenomics. Using deuterium-labeled serine and the RQMID-MS platform, we demonstrated that hypoxia impairs methyl group transfer from serine to histones due to the downregulation of the vitamin B transporter TCN2, which is critical for homocysteine remethylation and SAM synthesis. Despite this blockade in one-carbon metabolism, global histone methylation patterns were not uniformly suppressed. Instead, we observed site-specific changes driven by altered expression of methyltransferases and demethylases, particularly decreased KMT1F (H3K9 methylation) and KMT2B (H3K4 methylation) and increased KDM2A (H3K36 demethylation), KDM3A (H3K9 demethylation), and KMT5A/SETD8 (H4K20 monomethylation). These findings reveal that the histone methylation landscape under hypoxia is governed by a compensatory interplay between one-carbon metabolism and chromatin-modifying enzyme regulation. - Source: PubMed
Publication date: 2025/11/26
Tang HuiXu PeiHerring JasonZhang Kangling - Vitamin B12 deficiency is a health concern leading to neurological and hematological disorders with genetic factors. This study investigated the effects of polymorphisms in the Transcobalamin II (TCN2, rs1801198) gene and its receptor CD320 (rs2336573) on serum vitamin B12 levels, circulating TCN2 and CD320 levels, and basic hematological parameters. - Source: PubMed
Publication date: 2025/11/01
Bahtiyar NurtenKucuk Ataman BuketAydemir BirsenCinemre Deniz AhmetCinemre Gunes CihanKaracaer CengizAfsar LeylaSerinkan Fatma Behice