S100A9 _ Calgranulin-B _ MRP14 antigen

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899.25 €

Known as:: S100A9 _ Calgranulin-B _ MRP14 antigenic
Catalog number:: 'H00006280-P01-25
Product Quantity:: 25
Category:: -
Supplier:: ACR
Gene target:: S100A9 _ Calgranulin- MRP14 antigen

Related genes to: S100A9 _ Calgranulin-B _ MRP14 antigen

Gene:: S100A9 ^{NIH gene}
Name:: S100 calcium binding protein A9
Previous symbol:: CAGB, CFAG
Synonyms:: P14, MIF, NIF, LIAG, MRP14, MAC387, 60B8AG, CGLB
Chromosome:: 1q21.3
Locus Type:: gene with protein product
Date approved:: 1989-05-19
Date modifiied:: 2018-05-02

Related products to: S100A9 _ Calgranulin-B _ MRP14 antigen

Related articles to: S100A9 _ Calgranulin-B _ MRP14 antigen

Cross-species transcriptomics identify mineralocorticoid receptor pathway overactivation as a central driver of ocular rosacea.
Ocular rosacea (OR) is a chronic inflammatory disease of the ocular surface frequently associated with meibomian gland dysfunction (MGD), with limited therapeutic options and an underexplored pathophysiology. Here, we uncover the pivotal role of mineralocorticoid receptor (MR) pathway overactivation in driving MGD and OR. Analysis of eyelid tissues from OR patients revealed increased MR expression and altered local corticosteroid metabolism, associated with inflammation, fibrosis, and impaired meibocyte renewal. Using a transgenic rat model overexpressing human MR, we demonstrate that MR overactivation initiates subclinical MGD and, with aging or ultraviolet-B exposure, drives a full OR-like phenotype characterized by gland dropout, oxidative and mitochondrial stress, immune infiltration, epithelial barrier disruption, and secondary corneal damage. Cross-species transcriptomic integration of rat, human MGD, and rosacea datasets identified a conserved MR-dependent gene signature, highlighting S100A9 as a specific downstream target and biomarker of MR activation. Local pharmacological MR antagonism suppressed S100A9 expression. These findings establish MR overactivation as a unifying pathogenic driver of MGD and OR and identify MR blockade as a promising therapeutic strategy, with S100A9 as a candidate biomarker for patient stratification and treatment monitoring. - Source: PubMed
Publication date: 2026/04/16
Zhu LinxinYesilirmak NiluferRodrigues-Braz DanielaGélizé EmmanuelleLheure CoralieMorel XavierBourges Jean-LouisJaisser FrédéricZhao MinBehar-Cohen Francine
Preclinical efficacy of tasquinimod in myelodysplastic neoplasms: Restoring erythropoiesis and mitigating bone loss.
Myelodysplastic neoplasms (MDSs) are clonal disorders characterized by ineffective hematopoiesis, dysplasia, and a risk of transformation into acute myeloid leukemia. MDS is also associated with a higher incidence of osteoporosis, suggesting a complex interplay between hematopoiesis, the bone marrow (BM) microenvironment, and bone homeostasis. Targeting inflammation has emerged as a promising therapeutic strategy, particularly in lower risk MDS. Tasquinimod (TASQ) is a small-molecule inhibitor of the inflammatory alarmin S100A9, blocking its interaction with TLR4 and RAGE receptors. We investigated the efficacy of TASQ in modulating inflammation and improving disease phenotype using in vitro and in vivo MDS models. Immunofluorescence staining of human BM identified neutrophils and macrophages as primary S100A9 sources. Exposure of mesenchymal stromal cells (MSCs) to S100A9 induced Toll-like receptor 4 (TLR4) downstream signaling, resulting in increased expression of IRAK1, NF-κB-p65, interleukin-1β (IL-1β), IL-18, caspase 1, and PD-L1. These effects were effectively abolished by TASQ. Additionally, TASQ restored the disturbed MSC-mediated hematopoietic support, as demonstrated by increased numbers of cobblestone area-forming cells and colony-forming units. In NHD13 MDS mice, TASQ (30 mg/kg, 12 weeks) improved hemoglobin and red blood cell counts, but exerted no effect in wild-type (WT) mice. Additionally, TASQ improved bone microarchitecture by increasing trabecular number and bone volume, likely a result of reduced osteoclast activity. Our findings suggest that TASQ mitigates inflammasome activation in the MDS BM, improving erythropoiesis and bone health. These results provide a necessary preclinical basis for clinical trials in lower risk MDS patients, in whom anemia and osteoporosis often coexist. - Source: PubMed
Publication date: 2026/04/14
Wobus ManjaWeidner HeikeWehner RebekkaBaumann Anna-LenaMöbus KristinBalaian EkaterinaTörngren MarieVahtola ErikEriksson HelenaWinter SusannPlatzbecker UweChavakis TriantafyllosHofbauer Lorenz ChristianRauner MartinaBornhäuser MartinSockel Katja
Inhibition of S100A9 Mitigates Aging-Related Mitochondrial Dysfunction and Neurodegeneration in Parkinson's Disease.
Aging is the most important risk factor for Parkinson's disease (PD). S100A9, a calcium-binding protein, is closely related to a variety of aging-related diseases, but its role in the pathogenesis of PD is still unclear. This study aims to investigate the role of S100A9 in aging-related mechanisms in PD. C57BL/6J mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP; 15 mg/kg four times daily), followed by Paquinimod (a S100A9 inhibitor; 7 mg/kg, once a day for 7 days after model establishment, totaling 8 doses). We found that MPTP induced significant motor deficits and dopaminergic nerve damage, accompanied by up-regulation of p21 expression, down-regulation of Lamin B1 expression, and significant increases in SASP factors such as MMP9, IL-1α, IL-1β, and IL-6. Treatment with recombinant S100A9 protein induced senescence-like molecular alterations and reduced expression of mitochondrial biogenesis-associated genes in astrocytes in vitro. Inhibition of S100A9 effectively improved movement disorders, restore TH-positive fiber density, reduce the expression of cell senescence markers and SASP factors, and up-regulate mitochondrial function-related genes. Studies have shown that S100A9 plays a key bridge between aging and neurodegeneration in PD. Inhibition of S100A9 may be a potential therapeutic strategy to alleviate cell senescence and mitochondrial damage in PD. - Source: PubMed
Publication date: 2026/04/13
Tan Lu-LuMa Xiao-YuXia Yi-MengLi TingLi Ming-AnWu JianNie XinHuang Shu-BingCui ChunZhao Wei-JiangQiao Chen-MengShen Yan-Qin
COVID-19 severity biomarkers identified by transcriptomics: a scoping review.
Omics technologies, particularly transcriptomics, were widely used during the COVID-19 pandemic to investigate host and viral gene expression. Given the substantial number of studies published during this period, systematic reviews are essential for synthesising findings and identifying consistent patterns. - Source: PubMed
Publication date: 2026/04/15
Oliveira Thais TeixeiraMedeiros Viviane Priscila Barros deFreitas Júlia FirmeMelo Martins Silva GiovannaXavier Thiago Jesus da SilvaFassarella Agnez-Lima Lucymara
Integrated Genomic Analysis Reveals New Diagnostic Biomarkers and Immune Mechanisms for Polycystic Ovary Syndrome.
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder associated with metabolic dysregulation and chronic inflammation. This study employed bioinformatics approaches to analyze the roles of neutrophil extracellular traps (NETs)-related genes (NETRGs) and mitochondria-related genes (MRGs) in PCOS pathogenesis. - Source: PubMed
Publication date: 2026/04/08
Huang NingLou LuYun

S100A9 _ Calgranulin-B _ MRP14 antigen

Related genes to: S100A9 _ Calgranulin-B _ MRP14 antigen

Related products to: S100A9 _ Calgranulin-B _ MRP14 antigen

Related articles to: S100A9 _ Calgranulin-B _ MRP14 antigen

Cross-species transcriptomics identify mineralocorticoid receptor pathway overactivation as a central driver of ocular rosacea.

Preclinical efficacy of tasquinimod in myelodysplastic neoplasms: Restoring erythropoiesis and mitigating bone loss.

Inhibition of S100A9 Mitigates Aging-Related Mitochondrial Dysfunction and Neurodegeneration in Parkinson's Disease.

COVID-19 severity biomarkers identified by transcriptomics: a scoping review.

Integrated Genomic Analysis Reveals New Diagnostic Biomarkers and Immune Mechanisms for Polycystic Ovary Syndrome.