Ask about this productRelated genes to: MOBP antibody
- Gene:
- MOBP NIH gene
- Name:
- myelin associated oligodendrocyte basic protein
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-13
- Date modifiied:
- 2019-02-15
Related products to: MOBP antibody
Related articles to: MOBP antibody
- Progressive supranuclear palsy (PSP) is a tauopathy and has a multifactorial etiology. The genetic component comprises at least 15 genes with unrelated functions that increase risk for PSP with a high degree of certainty. The function of these genes in increasing risk for PSP is presently unknown. This study was undertaken to identify new pathological pathways of these genes/proteins in increasing risk for PSP. Identification of possible targets and pathways of these genes was investigated using publicly available databases. 13 out of 15 of the risk genes, i.e. , and target microtubules, and directly alter their function via variable mechanisms. We now present data that these pathways are predicted to involve common pathways strongly involving microtubule hemeostasis, such as vesicle transport of misfolded proteins to lysosomes and cellular export. Two genes ( and ) are not obviously directly targeting microtubules. Mutations of the risk genes interfere with microtubular function and/or structure as they relate to axon formation/integrity, axon transport, intracellular organelle transport and communication, and cellular, microtubule - guided waste management. Microtubules may be thought of as a conveyor belt for the distribution of nutrients and waste management. Taken together these alterations include an increased risk of tau precipitation (MAPT) and are molecular drivers of neuronal degeneration in PSP. Although microtubular dysfunction has long been documented in PSP mainly based on the findings related to MAPT, this is the first study of the effect of risk genes in PSP. We demonstrate that most of these genes (13/15) also affect microtubular structure and function. These genes/proteins may also be biased towards neurodegeneration in motor neurons. - Source: PubMed
Publication date: 2026/04/20
Donlon Timothy AMüller Ulrich - Myelin oligodendrocyte basic protein () is an abundant oligodendrocyte gene implicated in multiple neurodegenerative diseases. Genetic variation at the locus has been associated with risk for progressive supranuclear palsy (PSP), amyotrophic lateral sclerosis (ALS), frontotemporal lobar degeneration (FTD), corticobasal degeneration (CBD), Alzheimer's disease (AD), Lewy body dementia (LBD), and Creutzfeldt-Jakob disease (CJD). Epigenetically, promoter hypermethylation and reduced expression have been reported in multiple system atrophy (MSA). Although is thought to play a role in oligodendrocyte morphology and myelin structure, how genetic and epigenetic variation at this locus influences gene regulation and contributes to disease risk remains poorly understood across neurodegenerative disorders. Here, we investigated whether shared or disease-specific genetic mechanisms at converge on altered DNA methylation and expression across neurodegenerative disorders. We analysed variants using summary statistics from recent GWAS for ALS, PSP, FTD, LBD, PD, MSA, AD, and CJD. Colocalisation (COLOC and SuSiE-coloc) was used to test whether disease-associated variants overlapped between diseases, and with oligodendrocyte expression quantitative trait loci (eQTLs) and bulk brain methylation quantitative trait loci (mQTLs). To further investigate mQTL effects at this locus, rs1768208, a variant previously associated with PSP, was genotyped in an overlapping brain methylation cohort, allowing direct testing of genotype-methylation associations in frontal white matter tissue. ALS and PSP GWAS demonstrated strong association at , with most strongly associated SNPs (e.g. rs631312, rs616147, rs1768208) shared between both disorders. Colocalisation analyses indicated high posterior probability that ALS and PSP share the same causal variant, with weaker overlap with FTD. mQTL colocalisation highlighted cg15069948, located near an exon junction within , as strongly colocalising with the ALS/PSP risk variants. In complementary tissue analyses, rs1768208-T carriers showed hypomethylation at cg15069948 in PSP brains. No genotype-methylation effects were detected in MSA or Parkinson's disease. Together with prior evidence of promoter hypermethylation and reduced expression in MSA, our findings identify cg15069948 as a regulatory methylation site linking ALS/PSP risk variants to altered methylation, and support dysregulation as a shared feature of neurodegeneration. However, the underlying mechanisms appear disease-specific, highlighting the complexity of involvement of this gene across neurodegenerative disorders. - Source: PubMed
Publication date: 2026/03/27
Fodder KatherineMurthy Meghade Silva RohanRaj TowfiqueFarrell KurtHumphrey JackBettencourt Conceição - The expansion of intensive poultry farming has led to a substantial increase in antibiotic use, which, in turn, has promoted the accumulation of antibiotic resistance genes (ARGs). The chicken gut serves as a reservoir for these genes and provides favorable conditions for their horizontal transfer via mobile genetic elements, such as plasmids. Through this process, commensal bacteria can transfer ARGs to pathogens, facilitating their spread and increasing the risk of transmission to humans. In this study, long-read sequencing was used to characterize the plasmidome and resistome in 12 fecal samples from 3 houses of a commercial broiler chicken farm. All chickens received enrofloxacin in the first days of life, with one house additionally treated with sulfamethoxazole/trimethoprim combination. For comparison, metagenomic analysis using short-read sequencing was performed on the same samples. This study revealed the presence of various ARGs associated with resistance to 25 antibiotic classes. A strong genetic association between MOBP-type plasmids and fluoroquinolone resistance was observed within broiler chicken farms. Temporal trends indicated progressive mobilization of these ARGs, suggesting an increasing potential for horizontal gene transfer. While fluoroquinolone resistance expanded over time, diaminopyrimidine resistance remained stable despite the antibiotic treatment. Most ARGs were carried on small plasmids, and complete plasmid reconstructions ranged from 2.6 to 47.6 kb. Our findings demonstrate that plasmidome sequencing enables high-resolution detection of resistance-associated plasmids that may be overlooked by conventional metagenomic approaches. The observed patterns are consistent with an association between fluoroquinolone use in poultry farms and the presence of plasmid-mediated resistance genes with potential for horizontal dissemination.IMPORTANCEDespite the crucial role of plasmids in antimicrobial resistance (AMR) dissemination, studies focusing on plasmidomes, defined as the complete set of plasmids, remain limited. This study is the evidence that chicken farms, where fluoroquinolone treatment is a standard practice, act as an important reservoir of plasmid-mediated antibiotic resistance which may not be revealed by commonly used approaches. Combining a metagenomic approach with a focus on plasmids enhances our ability to understand the genetic context and mechanisms underlying AMR transmission. The findings emphasize the importance of targeted plasmid analysis to improve surveillance and risk assessment of AMR transmission in microbial ecosystems. - Source: PubMed
Publication date: 2026/03/26
Rysava MarketaStredanska KatarinaSchwarzerova JanaJakubickova MarketaCejkova DarinaAytan-Aktug DeryaOtani SariaDolejska MonikaPalkovicova Jana - Initial phases of multiple sclerosis (MS) are characterized by recurrent focal inflammation within the central nervous system associated with demyelination and variable subsequent remyelination, indicating that both injury and repair are ongoing within the same microenvironment. An array of pro-inflammatory molecules including tumor necrosis factor α (TNF) and interferon γ (IFNG) are implicated as contributing to oligodendrocyte (OL) lineage cell injury in MS and its models. Using OL lineage cells derived from human surgical samples, we observed that TNF and IFNG in combination enhanced ensheathment of synthetic nanofibers by mature OLs compared to those observed under control conditions or in the presence of individual cytokines, reaching levels comparable to those of A2B5+ late-stage progenitor cells. The combination reversed the individual cytokine mediated inhibition of A2B5+ cell ensheathment. Molecular analysis of the mature OL population identified increased expression of myelination relevant genes in the cytokine combination treated cells, of STAT and IRF transcription factors (TFs) that regulate many of these genes, and of mature OL structural genes (MOBP and CNP). TNF and IFNG combination also reduced expression of OPC signature genes in the mature OLs compared to IFNG alone. The combination effect on ensheathment was reversed using a JAK/STAT pathway inhibitor. The combination of TNF and IFNG induced a stronger immune signature in mature OLs compared to individual cytokines. These results emphasize the complex positive and negative interplay of inflammatory responses in the CNS and the potential for therapeutic modulation. - Source: PubMed
Publication date: 2026/03/11
Mohammadnia AbdulshakourCui Qiao-LingYaqubi MoeinBlaszczyk Gabriela JWeng ChaoHall Jeffery ADudley RoyStratton Jo AnneZandee StephanieKennedy Timothy ESrour MyriamAntel Jack P - Accurate blood pressure (BP) measurement is critical in patients with chronic kidney disease (CKD) due to its strong association with cardiovascular morbidity and progression of renal dysfunction. While ambulatory BP monitoring (ABPM) is considered the gold standard, it is often impractical in routine settings. This study compares manual office BP (MOBP), automated office BP (AOBP), and ABPM to evaluate diagnostic accuracy and clinical utility in CKD patients. - Source: PubMed
Publication date: 2026/03/09
Teja B Sai SuryaSrinath K MReddy R HareethBalineni AjithGanti EswarBasavegowda MadhuGottipati SrikarSri Pasam SnigdhaGullapalli SasiBattula Midhu Meghana