S100A9 predesign siRNA
- Known as:
- S100A9 predesign small interfearing RNA
- Catalog number:
- RI14689
- Product Quantity:
- 5 OD
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- S100A9 predesign siRNA
Related genes to: S100A9 predesign siRNA
- 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 predesign siRNA
Related articles to: S100A9 predesign siRNA
- Imiquimod (IMQ)-induced psoriasis-like mouse models are widely used for psoriasis research, but existing methods fail to sustain disease manifestation over time. This study explores the effect of different IMQ dosing frequencies on maintaining psoriasis symptoms in mice. - Source: PubMed
Publication date: 2026/04/23
Zhu HaoyueYu XiaohanWang YazhuoZhao NingQu BaoquanMa HuikeMeng YujiaoZhao JingxiaWang YanLi Ping - N6-methyladenosine (m6A) modifications are implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD), yet the precise role of the demethylase fat mass and obesity-associated protein (FTO) remains unclear. - Source: PubMed
Publication date: 2026/04/28
Xie BinChen QiongDai ZiyuPeng YunYou ShaojinHu ChengpingChen Xi - Macrophage-mediated inflammation has been implicated in the pathogenesis of liver fibrosis. Metabolic reprogramming involves the transition of macrophages from a proinflammatory M1 phenotype toward an anti-inflammatory M2 phenotype. S100A9 is highly expressed in activated macrophages and promotes M1 polarization; however, it is unknown whether S100A9 alters the polarization state of macrophages by regulating metabolism. This study revealed enhanced oxidative phosphorylation (OXPHOS) in -deficient bone marrow-derived macrophages (BMDMs) based on mitochondrial proteomics, characterized by increased mitochondrial fusion and elevated ATP production. Further phenotypic analysis showed that -deficient peritoneal macrophages and BMDMs exhibited an M2-like phenotype at the basal state and enhanced M2 polarization with IL-4/IL-13 stimulation, reflected by higher CD206 expression. Using the OXPHOS inhibitor oligomycin, we demonstrated that suppressing OXPHOS completely rescued the M2 polarization bias of the -deficient macrophages. Finally, we found that genetic deletion of S100A9 in myeloid cells protected against liver injury and fibrogenesis through increasing the proportion of hepatic CD206-positive M2-like anti-inflammatory macrophages in a mouse model. Our study uncovers a novel role of S100A9 in macrophage mitochondrial metabolism and phenotype reprogramming during liver fibrosis, and targeting macrophage S100A9 may be considered as a potential therapeutic strategy against liver fibrosis. - Source: PubMed
Publication date: 2026/04/28
Liu JinfangLiu RuixiShi YunweiSun YiZhang ZhenpengMao MingsongChang LeiZhang TaoHan ChunguangWu JunzhuXu Ping - Casein Kinase 2 (CK2) is a constitutively active kinase regulating proliferation and immune signaling and is frequently dysregulated in cancer, including acute myeloid leukemia (AML), making it a therapeutic target. CK2 comprises two catalytic subunits, CK2α or CK2α', with two regulatory β subunits. The role of CK2α, the predominant catalytic subunit and principal mediator of CK2 kinase activity in hematopoietic cells, in steady-state hematopoiesis remains undefined. To define how CK2α shapes hematopoietic cells, we used bone marrow and spleen tissue samples of wild type control and conditional knock out (KO) of CK2α ( ) in the hematopoietic compartment of transgenic mice. Using single-cell RNA sequencing, we profiled the transcriptomic changes associated with CK2α loss. Although HSC abundance was comparable between the control and CK2α-deficient samples, HSCs experienced the largest transcriptional response to CK2α loss among all cell types. CK2α-deficient HSCs displayed transcriptional remodeling for inflammatory and immune-associated programs, interferon signaling, and antigen presentation. Expression of inflammatory genes such as and , changed in opposite directions in bone marrow and spleen HSCs, demonstrating the transcriptional consequences of CK2α loss shaped by tissue context. Using a network-based approach, we identified immune-associated transcription factors , and AP-1 family members as regulatory hubs driving these inflammatory transcriptional states in CK2α-deficient HSCs. Cell-cell communication profiling revealed multiple gains and losses in ligand-receptor communication between the HSCs and their immune microenvironment in KO. Our findings identify CK2α as a regulator of immune transcriptional programs in HSCs and suggest that disruption of CK2 signaling influences stem cell behavior and immune activation in contexts relevant to hematologic malignancies and CK2-targeted cancer therapies. - Source: PubMed
Publication date: 2026/04/15
Valensi HannahRajaiah RajeshShanmugam MarudhuMuhammad DaniyalGolla UpendarMercer KatherineKarampuri AnushDovat SinisaBehura ChandrikaUzun Yasin - Polycystic ovary syndrome (PCOS) remains difficult to diagnose reliably, especially when clinical decisions rely heavily on ovarian morphology, which is often mis-interpreted. To address the need for more objective molecular indicators, we validated four serum proteins highlighted in earlier nLC-MS/MS based proteomic work, namely; Fibrinogen, S100A9, SERPINA3 and SERPINA6. The objective was to analyse differential expression of these proteins and evaluate the diagnostic performance by using ROC curves. - Source: PubMed
Publication date: 2026/04/23
Fatima SabeenKori Junaid AhmedVankwani SomaMirza Munazza RazaRehman Rehana