Thioredoxin-related transmembrane protein 2 TMX2
- Known as:
- Thioredoxin-related transmembrane protein 2 TMX2
- Catalog number:
- CH30
- Product Quantity:
- lmg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Thioredoxin-related transmembrane protein 2 TMX2
Related genes to: Thioredoxin-related transmembrane protein 2 TMX2
- Gene:
- TMX2 NIH gene
- Name:
- thioredoxin related transmembrane protein 2
- Previous symbol:
- TXNDC14
- Synonyms:
- PDIA12
- Chromosome:
- 11q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-04
- Date modifiied:
- 2016-02-01
Related products to: Thioredoxin-related transmembrane protein 2 TMX2
Related articles to: Thioredoxin-related transmembrane protein 2 TMX2
- The d-band center theory has long provided a useful framework for understanding hydrogen adsorption in HER electrocatalysis, yet its predictive capability becomes limited in half-metallic systems where spin asymmetry dominates the electronic structure. In such systems, hydrogen adsorption is expected to depend on spin-resolved dz2 orbital filling (n) rather than spin-averaged electronic states. Here, we show that n quantitatively correlates with the hydrogen adsorption Gibbs free energy (ΔG) in two-dimensional half-metal catalysts, as exemplified by transition-metal-doped FeP4 and TMX2 (TM = Cr, Mn, Ti, and V; X = S, Se, and I) monolayers. We demonstrate that hydrogen adsorption is governed by spin-selective orbital interactions: unfilled dz2 states in the metallic spin channel enhance H binding, whereas those in the insulating spin channel weaken adsorption. This competition leads to an optimal adsorption regime when n approaches 0.5, due to cooperative contributions from the two spin channels. These results clarify spin-dependent orbital contributions and reveal a clear correlation between catalytic activity and spin-polarized electronic structure. Spin-resolved dz2 orbital filling thus emerges as a useful design descriptor for HER electrocatalysts based on two-dimensional half-metallic materials. - Source: PubMed
Zhang Xiang-LongYang Zi-XuanLi LeiYu Li-JunElamri Fatima-ZahraLeng CanHuang Gui-FangHu WangyuHuang Wei-Qing - Previous studies evaluating bentonite in have largely employed high-dose AFB challenge models (≥2 ppm in the diet), whereas information on its efficacy under sub-acute contamination conditions is limited. This study evaluated the effects of a bentonite-based binder on growth performance and selected gross health-related indices in juvenile exposed to 250 ppb dietary AFB. In a 42-day feeding trial, 320 fish were randomly assigned to four treatments: a negative control (NC; no AFB or binder), a positive control (PC; 250 ppb AFB), and two AFB-contaminated diets supplemented with bentonite at 1 kg/ton (TMX-1) or 2 kg/ton (TMX-2). Dietary AFB exposure to 250 ppb impaired growth and feed intake and increased body-weight variability compared with the NC group ( < 0.01). Bentonite supplementation elicited inclusion-level-dependent responses. Fish fed TMX-2 had higher final body weight (+7.0%) and average daily gain (+7.9%) than those fed the PC diet ( < 0.01), whereas TMX-1 performed similarly to the PC group. Feed conversion ratio differed among treatments, with TMX-2 lower than TMX-1 ( = 0.02) but not significantly different from the NC or PC groups. Mortality, condition factor, body-weight variation and organosomatic indices did not differ among AFB-challenged treatments. These findings indicate that dietary bentonite supplementation, particularly at 2 kg/ton, partially alleviated adverse responses associated with sub-acute AFB exposure, primarily through improvements in final body weight and average daily gain, in juvenile under the conditions of the present study. - Source: PubMed
Publication date: 2026/08/03
Pineda LaneKhin May Moh MohSubramanian SaravananSwamy H V L NPhuc Hoang NhuLoc Tran Huu - Thioredoxin-related transmembrane protein 2 (TMX2)-related neurodevelopmental disorder (OMIM #618730) is an exceedingly rare autosomal recessive condition caused by biallelic pathogenic variants in , a gene encoding an endoplasmic reticulum (ER)-resident oxidoreductase involved in neuronal survival and cortical development. The condition is characterized by severe intellectual disability, microcephaly, spasticity, epilepsy, and cortical malformations, primarily polymicrogyria. We report a 13-month-old Moroccan male infant born to second-cousin consanguineous parents, presenting with severe global developmental delay, profound axial hypotonia, absent head control, and progressive microcephaly (head circumference 41 cm, < -3 standard deviation (SD)). Epilepsy was diagnosed at seven months of age and managed with valproic acid. Clinical examination revealed characteristic dysmorphic features, including microcephaly, a sloping forehead, bilateral strabismus, retrognathism, low-set ears and hairline, and bilateral second-third toe syndactyly - a feature not previously described in association with -related disorder. Brain MRI demonstrated bilateral frontoparietal polymicrogyria. Electroencephalography showed right hemispheric dysfunction with focal epileptic activity. Whole-exome sequencing identified a homozygous pathogenic missense variant in (NM_015959.4:c.614G>A; p.Arg205Gln), classified as pathogenic in ClinVar (VCV000804370), confirming the diagnosis. This case expands the phenotypic spectrum of -related disorder by documenting bilateral second-third toe syndactyly and highlights the diagnostic value of whole-exome sequencing in consanguineous families presenting with cortical malformations and severe neurodevelopmental delay. Early molecular diagnosis is essential for appropriate genetic counseling and multidisciplinary management. - Source: PubMed
Publication date: 2026/06/19
Baaziz AsmaeMdaghri Alaoui Asmaa - Ulcerative colitis (UC) remission is marked by gut microbiota restructuring, but how microbial metabolites influence immune-mediated tissue repair is unclear. Here, we demonstrate that oral vancomycin alleviates colitis symptoms in murine models, mirroring its clinical efficacy in inducing remission in patients with UC. Mechanistically, vancomycin's therapeutic effect is achieved by reducing deoxycholic acid (DCA). We reveal that DCA impairs mucosal repair driven by group 2 innate lymphoid cells (ILC2s) by inducing ER stress through direct binding to thioredoxin-related transmembrane protein 2 (TMX2). This interaction disrupts TMX2's role in protein folding, triggering unresolved unfolded protein response via hyperactivation of PERK/eIF2α signaling, which suppresses the production of pro-healing molecules by ILC2s. Pharmacological inhibition of PERK phosphorylation restores ILC2 function and accelerates colitis resolution. Our work uncovers a pathogenic microbiota/DCA/ILC2 axis that obstructs mucosal healing and positions vancomycin as a targeted strategy to eliminate DCA, thereby promoting UC remission. - Source: PubMed
Publication date: 2026/04/08
Tian QiuhengLiu HanGu XiangShen JingYuan XiZheng MengqiZhai YunjiaoChen YataiHan PenghuMa YangchunXin WeiMa HongyueLi YuWang SihanGuo LeiYuan DetianYu YanboLi Shiyang - Thioredoxin-related transmembrane proteins (TMXs) of the endoplasmic reticulum (ER) determine not only redox conditions within the ER lumen but also the formation and function of ER-mitochondria membrane contact sites (ERMCS). The presence of cytosolic, reactive oxygen species (ROS)-derived redox nanodomains at ERMCS suggests TMXs could also control these. The prime candidate for such a function is TMX2, the sole TMX family protein with a cytosolic thioredoxin domain. Indeed, TMX2 controls the extent of ERMCS through interaction with outer mitochondrial membrane proteins, including TOM70. Assisted by cytosolic peroxiredoxins, TMX2 moderates the sulfenylation of the TOM70 C residue. Thereby, TMX2 reduces mitochondrial Ca uptake and metabolism. Accordingly, mutation of the TMX2 gene in cells from a patient with a neurodevelopmental disorder with microcephaly, cortical malformations, and spasticity (NEDMCMS) results in hyperactive mitochondria. In a fly in vivo NEDMCMS model, TMX2 knockdown manifests predominantly in glial cells, where it prevents seizure-like behavior. - Source: PubMed
Publication date: 2025/10/31
Chen JunshengYap Megan CBassot ArthurPascual Danielle MMakio TadashiZimmermann JannikMast HeatherBhat RakeshFleury Samuel GFan YuxiangBuzatto Adriana ZardiniMoore JackBallanyi KlausLi LiangOverduin MichaelLemieux M JoanneLemieux HélèneMancini Grazia M SMorgan BruceMarcogliese Paul CSimmen Thomas