Ask about this productRelated genes to: LIN7C Blocking Peptide
- Gene:
- LIN7C NIH gene
- Name:
- lin-7 homolog C, crumbs cell polarity complex component
- Previous symbol:
- -
- Synonyms:
- MALS-3, Lin7c, LIN-7C, LIN-7-C, VELI3, FLJ11215
- Chromosome:
- 11p14
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-19
- Date modifiied:
- 2016-02-22
Related products to: LIN7C Blocking Peptide
Related articles to: LIN7C Blocking Peptide
- Schizophrenia (SCZ) is a chronic mental disorder with significant cognitive deficits and social dysfunction. Diagnostic biomarkers remain a challenge in the disease due to its heterogeneity. Exosomes, enriched for neuron-derived contents and accessible obtained from peripheral blood, are promising for biomarker discovery in schizophrenia. However, there are still scarce data characterizing the exosome proteins profile of schizophrenia. - Source: PubMed
Publication date: 2025/06/23
Sun XiaoxiaoQiu YuyingJi LijieLi MeijuanWang JiayueSu QiaoXuekelaiti ZaiminaBi FuyouLi Jie - Solute carrier (SLC) transporters form a protein superfamily that enables transmembrane transport of diverse substrates including nutrients, ions and drugs. There are about 450 different SLCs, residing in a variety of subcellular membranes. Loss-of-function of an unusually high proportion of SLC transporters is genetically associated with a plethora of human diseases, making SLCs a rapidly emerging but challenging drug target class. Knowledge of their protein environment may elucidate the molecular basis for their functional integration with metabolic and cellular pathways and help conceive pharmacological interventions based on modulating proteostatic regulation. We aimed at obtaining a global survey of the SLC-protein interaction landscape and mapped the protein-protein interactions of 396 SLCs by interaction proteomics. We employed a functional assessment based on RNA interference of interactors in combination with measurement of protein stability and localization. As an example, we detail the role of a SLC16A6 phospho-degron and the contributions of PDZ-domain proteins LIN7C and MPP1 to the trafficking of SLC43A2. Overall, our work offers a resource for SLC-protein interactions for the scientific community. - Source: PubMed
Publication date: 2025/05/12
Frommelt FabianLadurner ReneGoldmann UlrichWolf GernotIngles-Prieto AlvaroLineiro-Retes EvaGelová ZuzanaHopp Ann-KatrinChristodoulaki EiriniTeoh Shao ThingLeippe PhilippSantini Brianda LRebsamen ManueleLindinger SabrinaSerrano IciarOnstein SvenjaKlimek ChristophBarbosa BarbaraPantielieieva AnastasiiaDvorak VojtechHannich Thomas JSchoenbett JulianSansig GillesMocking Tamara A MOoms Jasper FIJzerman Adriaan PHeitman Laura HSykacek PeterReinhardt JuergenMüller André CWiedmer TabeaSuperti-Furga Giulio - In epithelia, apicobasal cell polarization is closely linked to cell-cell contact formation, both controlled by the conserved Crumbs (CRB) complex, which includes the transmembrane protein Crumbs (CRB3a) and adapter proteins PALS1, PATJ, and LIN7c. In MDCK II cells, a model for cell polarization, depletion of PALS1 - which binds to all CRB components - leads to defective cell polarization and improper distribution of tight junction proteins, resulting in severe epithelial barrier defects in 3D cyst models. This study investigated whether this phenotype is associated with transcriptional changes by analyzing wildtype (WT) and PALS1 knockout (KO) MDCK II cell lines grown under non-confluent conditions and in 3D cyst cultures. Our results indicate that the transition from non-confluent cells to 3D cysts involves numerous differentially expressed genes (DEGs) in both WT and KO cells. Importantly, the analyses revealed significant overlaps between WT and KO cells in their maturation processes, suggesting that most identified DEGs are linked to differentiation from non-confluent to polarized MDCK cells and likely not a result of PALS1 deficiency. Gene Ontology (GO) enrichment and over-representation analyses using REACTOME and KEGG databases confirmed these similarities. In contrast, the direct comparison of WT and KO cells at the two stages showed fewer DEGs and overlaps in associated biological processes and signaling pathways. DEGs associated with the 3D stage, in which the phenotype manifests, contain DEGs and pathways that were predominantly linked to cell cycle linked processes, centromere assembly, or DNA replication. Furthermore, the transcription of genes encoding key junction proteins, additional polarity proteins, and cell-substrate interaction proteins is less affected by the loss of PALS1, indicating that PALS1 influences the transcriptional profiles in epithelial cells as a modulating factor. - Source: PubMed
Publication date: 2024/11/29
Schughart KlausMöller-Kerutt AnnikaHöffken VerenaNedvetsky PavelGroh Ann-ChristinBraun Daniela AnnePavenstädt HermannWeide Thomas - Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with exposure to repetitive head impacts, which is susceptible in elderly people with declined mobility, athletes of full contact sports, military personnel and victims of domestic violence. It has been pathologically diagnosed in brain donors with a history of repetitive mild traumatic brain injury (rmTBI), but cannot be clinically diagnosed for a long time. By the continuous efforts by neuropathologists, neurologists and neuroscientists in recent 10 years, an expert consensus for the diagnostic framework of CTE was proposed in 2021 funded by the National Institute of Neurological Disorders and Stroke. The new consensus contributes to facilitating research in the field. However, it still needs to incorporate biomarkers to further refine and validate the clinical diagnostic criteria. From this, a single-center, observational cohort study has been being conducted by Tianjin Medical University General Hospital since 2021. As a pilot study of this clinical trial, the present research recruited 12 pairs of gender- and age-matched rmTBI patients with healthy subjects. Their blood samples were collected for exosome isolation, and multi-omics screening to explore potential diagnostic biomarkers in blood and its exosomes. The expression level of CHL1 protein, KIF2A mRNA, LIN7C mRNA, miR-297, and miR-1183 in serum and exosomes were found to be differentially expressed between groups. Besides, serum and exosomal CHL1, KIF2A, and miR-1183, as well as exosomal miR-297 were further verified as potential biomarkers for CTE by low-throughput assays. They are expected to contribute to establishing a novel set of CTE diagnostic signatures with classic neurodegenerative indicators in our future study, thereby updating the consensus diagnostic criteria for CTE by incorporating new evidence of the biomarkers. - Source: PubMed
Publication date: 2022/11/07
Ge XintongGuo MengtianLi MeimeiZhang ShishuangQiang JunlianZhu LuoyunCheng LuLi WenzhuWang YanYu JinwenYin ZhenyuChen FanglianTong WenLei Ping - The present study revealed that palmitic acid (PA) treatment induced epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells, which are involved in the progression of proliferative vitreoretinopathy (PVR). ARPE-19 cells were treated with PA followed by miRNA screening and EMT marker detection using qRT-PCR. Then, miR-124 mimic or inhibitor was transfected into ARPE-19 cells to explore the role of miR-124 on the EMT of ARPE-19 cells using transwell assay. The underlying mechanism of miRNA were predicted by bioinformatics method and confirmed by luciferase activity reporter assay. Furthermore, gain-of-function strategy was also used to explore the role of LIN7C in the EMT of ARPE-19 cells. The expression of miRNA or mRNA expression was determined by qRT-PCR and the protein expression was determined using western blot assay. The result presented that PA reduced the expression of E-cadherin/ZO-1 whilst increasing the expression of fibronectin/α-SMA. In addition, PA treatment enhanced the expression of microRNA (miR)-124 in ARPE-19 cells. Overexpression of miR-124 enhanced PA-induced upregulation of E-cadherin and ZO-1 expression and downregulation of fibronectin and α-SMA. Moreover, miR-124 mimic also enhanced the migration of ARPE-19 cells induced by PA treatment. Inversely, miR-124 inhibitor presented opposite effect on PA-induced EMT and cell migration in ARPE-19 cells. Luciferase activity reporter assay confirmed that Lin-7 homolog C (LIN7C) was a direct target of miR-124 in ARPE-19 cells. Overexpression of LIN7C was found to suppress the migration ability and expression of fibronectin and α-SMA, while increasing expression of E-cadherin and ZO-1; miR-124 mimic abrogated the inhibitive effect of LIN7C on the EMT of ARPE-19 cells and PA further enhanced this abolishment. Collectively, these findings suggest that miR-124/LIN7C can modulate EMT and cell migration in RPE cells, which may have therapeutic implications in the management of PVR diseases. - Source: PubMed
Publication date: 2022/06/01
Han Xiao-DongJiang Xu-GuangYang MinChen Wen-JunLi Li-Gang