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Last update 23 Jan 2025

JCHAIN

Last update 23 Jan 2025

Basic Info

Synonyms

IGCJ, IGJ, Immunoglobulin J chain

+ [3]

Introduction

Serves to link two monomer units of either IgM or IgA. In the case of IgM, the J chain-joined dimer is a nucleating unit for the IgM pentamer, and in the case of IgA it induces dimers and/or larger polymers. It also helps to bind these immunoglobulins to secretory component.

Drugs associated with JCHAIN

WO2023158307

Patent Mining

Target

JCHAIN

Mechanism-

Active Org.

Academisch Ziekenhuis Maastricht

Originator Org.

Academisch Ziekenhuis Maastricht

Active Indication

Hematologic Diseases [+3]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with JCHAIN

100 Translational Medicine associated with JCHAIN

0 Patents (Medical) associated with JCHAIN

210

Literatures (Medical) associated with JCHAIN

01 Feb 2025·International Journal of Laboratory Hematology

Application of Gene Expression Microarray for the Classification of Ph‐Like B‐Cell Acute Lymphoblastic Leukemia

Article

Author: Pakakasama, Samart ; Pongphitcha, Pongpak ; Chareonsirisuthigul, Takol ; Thangrua, Nonthaya ; Chutipongtanate, Somchai ; Siriboonpiputtana, Teerapong ; Mukda, Ekchol ; Rerkamnuaychoke, Budsaba ; Korkiatsakul, Veerawat

ABSTRACTIntroductionPh‐like ALL has gene expression profile similar to Ph‐positive ALL but without the BCR::ABL1 fusion. The disease presents higher rates of severe clinical features and is associated with unfavorable outcomes. There is still no standard pipeline for molecular characterization of the disease, and no valid predictor gene panel is available worldwide.MethodsWe performed expression microarray on 25 B‐cell ALL and 6 Ph‐positive B‐cell ALL to cluster and identify the transcriptional signature of Ph‐like ALL. qRT‐PCR was used to confirm the expression of candidate genes.ResultsFour out of 25 samples (16%) shared gene expression signatures related to and clustered with control Ph‐positive samples. Analysis of genes differentially expressed in Ph‐like B‐cell ALL and evidentially functional in normal blood cell development and leukemogenesis, we selected genes as potential biomarkers for Ph‐like B‐cell ALL in our dataset: ADGRE2, CD9, EPHA7, FAM129C, TCL1A, and VPREB1. Those genes were filtered by Ph‐like gene signatures obtained from distinct reliable data, resulting in five genes, CA6, CHN2, JAK1, JCHAIN, and PON2, selected for validation by qRT‐PCR. The Ct values of genes, including CA6 (p = 0.0017), PON2 (p = 0.0210), TCL1A (p = 0.0064), and VPREB1 (p = 0.0338), were significant in Ph‐like ALL. GSEA analysis identified VPREB1 as enrichment in the KRAS signaling pathway, and several genes that interact with VPREB1 were reported as critical molecules involved in the leukemogenesis of B‐cell ALL.ConclusionIn summary, we demonstrate using a gene expression microarray for classifying Ph‐like B‐cell ALL and highlight VPREB1 as a potential biomarker for this disease.

01 Jan 2025·Neurology Neuroimmunology & Neuroinflammation

Proteomics Reveals Age as Major Modifier of Inflammatory CSF Signatures in Multiple Sclerosis

Article

Author: Held, Friederike ; Hemmer, Bernhard ; Makarov, Christine ; Flaskamp, Martina ; Berthele, Achim ; Grummel, Verena ; Gasperi, Christiane

BACKGROUND AND OBJECTIVESMultiple sclerosis (MS) can start as relapsing or progressive. While their clinical features and treatment responses are distinct, it has remained uncertain whether their pathomechanisms differ. A notable age-related effect on MS phenotype and response to immunotherapies is well acknowledged, but the underlying pathophysiologic reasons are yet to be fully elucidated. We aimed to identify disease-specific and age-related proteomic signatures using a comprehensive targeted proteomic analysis.METHODSIn our retrospective cohort study, we analyzed the CSF and serum proteome of age-matched individuals with treatment-naïve relapsing-remitting and primary progressive MS, neurologic controls (NC), and individuals with neuroborreliosis using targeted proteomics and validated findings in an independent cohort. Proteomic results were integrated with clinical and laboratory covariates.RESULTSAmong 2,500 proteins, 47 CSF proteins were distinct between individuals with MS (n = 60) and NC (n = 20), with a subset also differing from those with neuroborreliosis (n = 8). We identified MS-associated proteins, including novel candidate biomarkers such as LY9 and JCHAIN, and putative treatment targets, such as SLAMF7, BCMA, and IL5RA, for which drugs are already licensed in other indications. The CSF proteome differences between relapsing and progressive MS were minimal, but major changes were noted in individuals older than 50 years, indicating a shift from MS-associated inflammatory to age-related protein signature. NEFL was the only serum protein that differed between individuals with MS and controls.DISCUSSIONThis study unveils a unique CSF proteomic signature in MS, providing new pathophysiologic insights and identifying novel biomarker candidates and potential therapeutic targets. Our findings highlight similar immunologic mechanisms in relapsing and progressive MS and underscore aging's profound effect on the intrathecal immune response. This aligns with the observed lower efficacy of immunotherapies in the elderly, thus emphasizing the necessity for alternative therapeutic approaches in treating individuals with MS beyond the age of 50.

01 Aug 2024·International Journal of Rheumatic Diseases

IGJ depletion suppresses proliferation, inflammation, and motility of rheumatoid arthritis fibroblast‐like synoviocytes via targeting NF‐κB pathway

Article

Author: Xuan, Dan ; Liu, Ruitao ; He, Qian ; Qiang, Fuyong ; Sheng, Jun

AbstractObjectiveTo investigate the impact of IGJ on the proliferation, inflammation, and motility of rheumatoid arthritis (RA) fibroblast‐like synoviocytes and elucidate the underlying mechanism.MethodsThe expression of IGJ RA fibroblast‐like synoviocytes was assessed using immunoblot and qPCR. Cell growth was evaluated using CCK‐8 and FCM assays. The effects on inflammatory response were determined by ELISA and immunoblot assays. Cell motility was assessed using transwell and immunoblot assays. The mechanism was further confirmed using immunoblot assays.ResultsIGJ expression was found to be elevated in fibroid synovial cells of RA. IGJ ablation inhibited the growth of MH7A cells and suppressed the inflammatory response. Knockdown of IGJ also blocked cell motility. Mechanically, the knockdown of IGJ suppressed the NF‐κB axis in MH7A cells.ConclusionIGJ suppresses RA in fibroblast‐like synoviocytes via NF‐κB pathway.

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JCHAIN

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