Ask about this productRelated genes to: LRRTM1 antibody
- Gene:
- LRRTM1 NIH gene
- Name:
- leucine rich repeat transmembrane neuronal 1
- Previous symbol:
- -
- Synonyms:
- FLJ32082
- Chromosome:
- 2p12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-22
- Date modifiied:
- 2014-11-18
Related products to: LRRTM1 antibody
Related articles to: LRRTM1 antibody
- Sinonasal tumours are rare entities presenting with non-specific symptoms, therefore being often misinterpreted. The present study aimed to evaluate if the 13-gene DNA Methylation assay for early cancer detection already assessed in the oral cavity, was also useful in nasal cavity tumours. The case series consisted of 93 patients (63 males/30 females), 49 with malignant tumours, 14 with benign/borderline tumours, 34 as control series with 33 inflammatory polyps and one fungus ball. We collected one flocked swab from the lesion and one from the contralateral nasal cavity. All sinonasal cancer cases were evaluated by bisulfite next generation DNA sequencing, investigating the following genes: ZAP70, ITGA4, KIF1A, PARP15, EPHX3, NTM, LRRTM1, FLI1, MIR193, LINC00599, MIR296, TERT, GP1BB. To evaluate the performance of the methylation assay, a specific methylation score was calculated for each sample using linear discriminant analysis, with a predefined positivity threshold of 1.0615547. The association between diagnosis and methylation score positivity was evaluated through Fisher's exact test and calculation of risk ratios with 95% confidence intervals. Additionally, dimensionality reduction techniques were employed to explore the structure of the dataset and assess the ability of methylation profiles to distinguish between different pathological conditions. The 13-gene DNA Methylation scored positive in 42/49 malignant tumours; We included also 14 benign/borderline tumours of which 11 scored positive. Among 33 inflammatory polyps, 24 scored negative, as well as 64/70 normal contralateral mucosa and one fungus ball. Therefore, excluding benign/borderline tumours, the detected sensitivity was 85.7% and specificity 85.6% (AUC: 0.878). - Source: PubMed
Publication date: 2026/01/29
Morandi LucaFarneti PaoloLeucci Anna CaterinaQuerzoli GiuliaMelotti SofiaCamagni AngelaGalli PaoloSollini GiacomoFranchi AlessandroTonon CaterinaLodi RaffaelePasquini ErnestoFoschini Maria Pia - Previous observational studies have indicated a significant correlation between plasma proteome composition and cataract pathological status; however, the direction of causality remains uncertain. In light of the aforementioned findings, the present study employs a bidirectional two-sample Mendelian randomisation strategy, with the objective of elucidating the direct causal link between plasma proteome changes and cataract development. Following rigorous data analysis and validation, a series of plasma proteins were identified as being strongly associated with cataract risk. These included ILF3, FAM171A1, ARHGEF2, LPR1B, CRYGD, GLT8D1, ARHGEF10 and LRRTM1, all of which were confirmed to be potential risk factors for cataract. In contrast, proteins such as MXRA7, ZHX3, SPAG11B, ARID1A, DNASE1L2, COX7A1 and EEF2K were found to exert a protective effect against cataract. To gain further insight into the specific mechanisms by which these causally related proteins contribute to cataract pathology, we subsequently performed an exhaustive bioinformatics analysis. This analysis not only deepened our understanding of the functional properties of these proteins, but also revealed their possible involvement in signalling pathways and molecular interactions, thereby providing new insights into the pathogenesis of cataract. - Source: PubMed
Publication date: 2025/12/17
Han XuanWang JinyanSu XiaojuanGuo XingyuYe Hejiang - Pyrethroid pesticides have been associated with neurodevelopmental disorders including attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). While behavioral effects of pyrethroid exposure have been previously reported, the underlying mechanisms remain unclear. Here, we hypothesized that exposure to deltamethrin (DM), a widely used pyrethroid pesticide known for its neurotoxicity during early developmental stages, induces brain dysfunction through alterations in brain-derived extracellular vesicle (BDEV) signaling. Using a well-established rodent model of early life DM exposure within the recommended no observable effect level, we isolated BDEVs from postnatal 30-day-old vehicle-exposed (control) and DM-exposed mice using a differential sucrose density gradient. Following ZetaView nanoparticle tracking and electron microscopy characterization, quantitative mass spectrometry-based proteomics revealed 89 differentially expressed proteins (DEPs) in BDEVs from DM exposed animals compared to control BDEVs. Bioinformatic analysis identified convergence of DEPs on pathways associated with mitochondrial function and synaptic plasticity. PKH67-green conjugated BDEVs derived from either control or DM-exposed mice were bilaterally injected intracerebroventricularly into naive adult mice, and the brain distribution of labeled BDEVs was verified prior to extracellular field recording experiments. Strikingly, long-term potentiation (LTP) at CA3-CA1 hippocampal synapses, a functional correlate of learning and memory, was intact in control BDEVs but absent in naive mice receiving BDEVs from DM exposed mice. Notably, exogenously delivering LRRTM1, one of the DEPs found in DM BDEVs, disrupts synaptic transmission in CA1 neurons consistent with impaired LTP. Thus, differentially regulated signaling in BDEVs represents a novel mechanism of DM neurotoxicity. - Source: PubMed
Publication date: 2024/12/31
Koff LeandraDi Re JessicaChand SubhashAvchalumov YosefNguyen Nghi MBaumgartner Timothy JSingh Aditya KGoode Nana AMarosi MateHallberg Lance MAmeredes Bill TGreen Thomas AYelamanchili Sowmya VPendyala GuruduttLaezza Fernanda - The mechanism of long-term depression (LTD), a cellular substrate for learning, memory, and behavioral flexibility, is extensively studied in Schaffer collateral (SC) synapses, with inhibition of autophagy identified as a key factor. SC inputs terminate at basal and proximal apical dendrites, whereas distal apical dendrites receive inputs from the temporoammonic pathway (TAP). Here, we demonstrate that TAP and SC synapses have a shared LTD mechanism reliant on NMDA receptors, caspase-3, and autophagy inhibition. Despite this shared LTD mechanism, proximal apical dendrites contain more autophagosomes than distal apical dendrites. Additionally, unlike SC LTD, which diminishes with age, TAP LTD persists into adulthood. Our previous study shows that the high autophagy in adulthood disallows SC LTD induction. The reduction of autophagosomes from proximal to distal dendrites, combined with distinct LTD inducibility at SC and TAP synapses, suggests a model where the differential distribution of autophagosomes in dendrites gates LTD inducibility at specific circuits. - Source: PubMed
Publication date: 2023/07/28
Keary Kevin MGu Qin-HuaChen JijiLi Zheng - Multiple trans-synaptic complexes organize synapse development, yet their roles in the mature brain and cooperation remain unclear. We analyzed the postsynaptic adhesion protein LRRTM1 in the prefrontal cortex (PFC), a region relevant to cognition and disorders. LRRTM1 knockout (KO) mice had fewer synapses, and we asked whether other synapse organizers counteract further loss. This determined that the immunoglobulin family member SynCAM 1 controls synapse number in PFC and was upregulated upon LRRTM1 loss. Combined LRRTM1 and SynCAM 1 deletion substantially lowered dendritic spine number in PFC, but not hippocampus, more than the sum of single KO impairments. Their cooperation extended presynaptically, and puncta of Neurexins, LRRTM1 partners, were less abundant in double KO (DKO) PFC. Electrophysiology and fMRI demonstrated aberrant neuronal activity in DKO mice. Further, DKO mice were impaired in social interactions and cognitive tasks. Our results reveal concerted roles of LRRTM1 and SynCAM 1 across synaptic, network, and behavioral domains. - Source: PubMed
Publication date: 2023/01/28
de Arce Karen PerezRibic AdemaChowdhury DhrubajyotiWatters KatherineThompson Garth JSanganahalli Basavaraju GLippard Elizabeth T CRohlmann AstridStrittmatter Stephen MMissler MarkusHyder FahmeedBiederer Thomas