Ask about this productRelated genes to: PTPRM antibody
- Gene:
- PTPRM NIH gene
- Name:
- protein tyrosine phosphatase receptor type M
- Previous symbol:
- PTPRL1
- Synonyms:
- RPTPU, hR-PTPu
- Chromosome:
- 18p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-23
- Date modifiied:
- 2019-02-14
Related products to: PTPRM antibody
Related articles to: PTPRM antibody
- The co-occurrence of plastic-derived particles and plastic-associated chemicals represents an emerging toxicological concern, yet their combined neurotoxicity remains insufficiently understood. Here, we evaluated whether repeated oral concurrent exposure to polyethylene nanoplastics (PE-NPs) and butyl benzyl phthalate (BBP) aggravates neurotoxic outcomes and characterized associated cell-type-resolved brain responses. In HT-22 neuronal cells, concentration-response matrix analysis revealed a positive interaction pattern between PE-NPs and BBP. A 90-day oral exposure model was then established in mice using pristine 50 nm PE-NPs, BBP, and their combination. Compared with single exposures, concurrent exposure caused more pronounced impairment in locomotor/exploratory behavior and spatial learning, accompanied by aggravated hippocampal neuronal and synaptic injury, neurotransmitter disturbance, enhanced glial reactivity, and reduced tight-junction-associated markers. Whole-brain single-nucleus RNA sequencing of control and co-exposure groups identified co-exposure-associated transcriptional alterations across neuronal, glial, and endothelial populations, involving synaptic organization, mitochondrial bioenergetics, glial/complement responses, and neurovascular barrier-related processes. Cell-cell communication analysis further suggested contraction of neuronal adhesion/trophic and vascular-associated signaling networks under the co-exposure condition. Targeted qRT-PCR validation using all four exposure groups supported representative snRNA-seq-derived candidates, including decreased Rbfox3, Rims1, Erbb4, Nrg1, Ptprm, and Cldn5 and increased Apoe and C1qa, with significant PE-NP × BBP interactions detected for Apoe, C1qa, and Cldn5. Overall, these findings show that concurrent PE-NP and BBP exposure aggravated neurotoxic outcomes and highlight the need to consider mixed plastic-derived contaminants in neurotoxicity assessment. - Source: PubMed
Publication date: 2026/08/12
Lu YitongRen HoudaoLv ZhongtingZhang TiehuaZhang JieRen Li - Hypoxic pulmonary hypertension (HPH) is a progressive chronic disorder characterized by elevated mean pulmonary arterial pressure. It severely impairs right ventricular function and ultimately causes right ventricular failure. Clarifying the complex pathogenesis of HPH remains a critical challenge. - Source: PubMed
Publication date: 2026/08/10
Shen Yan-YingChen Yi-BingLi XinXu XiangGuo GeLi Han-LuYao Yong-MingLiu Chun-Lei - Estrogen-related receptor gamma (ERRγ) drives an exercise mimicking aerobic gene program in the skeletal muscle that could be beneficial in aging. We have investigated the effect of chronic ERRγ activation on minimizing sarcopenia. - Source: PubMed
Publication date: 2026/06/11
Sopariwala D HDeBruine APoliakova SMosa EMann ECitu CituZhao ZhongmingKumar ANarkar V A - International guidelines recommend molecular profiling for patients with advanced biliary tract cancer (BTC) eligible for systemic treatment, but the utility of deep, multi-omic approaches remains underexplored. - Source: PubMed
Publication date: 2026/05/08
Nichetti FHoffmeister PKorell FHuellein JUhrig SRübsam MSchwab MTeleanu M-VJenzer MKreutzfeld SHorak PKonietzke PGlimm HHeining CRieke DKindler TSpringfeld CHeilig C EHübschmann DFröhling SKöhler B C - 18p deletion syndrome (OMIM #146390) displays a variable clinical spectrum due to differences in deletion size, position, and penetrance. While several classical phenotypes have been linked to specific genomic regions, many genotype-phenotype correlations remain elusive. Here we present a 30-year-old female patient with the classical features of 18p deletion syndrome, along with reproductive endocrine abnormalities, including elevated prolactin levels and diminished ovarian reserve. Chromosomal microarray revealed a 13.85 Mb deletion at 18p (arr[GRCh37]18p11.32p11.21(136,228_13,986,303)x1). To better delineate the clinical and molecular cytogenetic findings associated with monosomy 18p and explore genotype–phenotype correlations, we also reviewed 41 reported cases (including the present case) with confirmed genomic deletions indexed in the PubMed database between 2010 and 2025. The results showed that terminal deletions were most common (66%), with interstitial deletions accounting for 32%. Among cases with breakpoint data, 71% had the proximal breakpoint at 18p11.21, and 63% of deletions exceeded 10-Mb. Reverse phenotyping identified candidate intervals for multiple phenotypes: a 1.2-Mb region (chr18:1,852,498_3,039,186, hg19) was linked to white-matter abnormalities and ptosis, and a 5.9-Mb region (chr18:5,416,774_11,286,578, hg19) was associated with white-matter abnormalities, ptosis, and autoimmune susceptibility. PIEZO2 and SMCHD1, located within the 5.9 Mb and 1.2 Mb regions respectively, are potential candidate genes for ptosis. PTPRM in 5.9 Mb region is a potential candidate gene for causing autoimmune disorders. The genitourinary abnormalities presented here constitute a useful addition to the phenotypic spectrum of 18p deletion syndrome. However, their definitive inclusion in the syndrome’s clinical profile requires confirmation by future studies. These data expand the recognized clinical manifestations and refines potential candidate regions associated with key phenotypes, thereby providing a valuable resource for improved genetic counseling and future investigations into potential molecular targets. - Source: PubMed
Publication date: 2026/02/23
Cheng XiaXu LiangWu JiataoZhang LiWei XuetingMin ShengpingLiao Yaping