FOSL2 Mouse Monoclonal Antibody
- Known as:
- FOSL2 Mouse Monoclonal Antibody
- Catalog number:
- BIN-002355-M03
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FOSL2 Mouse Monoclonal Antibody
Related genes to: FOSL2 Mouse Monoclonal Antibody
- Gene:
- FOSL2 NIH gene
- Name:
- FOS like 2, AP-1 transcription factor subunit
- Previous symbol:
- -
- Synonyms:
- FRA2, FLJ23306
- Chromosome:
- 2p23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-02
- Date modifiied:
- 2016-10-05
Related products to: FOSL2 Mouse Monoclonal Antibody
Related articles to: FOSL2 Mouse Monoclonal Antibody
- Congenital aniridia, a rare disorder caused by PAX6 haploinsufficiency, is characterized by progressive, vision-threatening aniridia-associated keratopathy (AAK) with limbal epithelial dysfunction and chronic inflammation. Downregulation of fatty acid binding protein 5 (FABP5) has been reported in conjunctival cells of congenital aniridia patients and in limbal epithelial cells (LECs) of the PAX6 siRNA knockdown model. We aimed to investigate the effects of FABP5 deficiency on LECs gene expression, without or with inflammatory stimuli. To achieve FABP5 knockdown, human primary LECs were transfected with FABP5 siRNA, using Lipofectamine 2000. Inflammation was induced 48 hours after transfection by incubating cells with 2 µg/mL lipopolysaccharides (LPS) or 1 ng/ml IL-1β. Thereafter, gene and protein levels were examined using qPCR, Western blot and ELISA. Significant downregulation of PAX6, KRT3 and MMP2 and upregulation of KRT12 mRNA level was observed upon FABP5 knockdown (p ≤ 0.022). Under inflammatory conditions (IL-1β or LPS treatment), FABP5 knockdown led to reduced PAX6, FOSL2, IL-6, PTGES2, KRT3, MAPK3 and MMP2 (p ≤ 0.048) and increased VEGFα and CRABP2 mRNA expression levels compared to control LECs (p ≤ 0.034). Following FABP5 knockdown, reduced PAX6, IL-6 and KRT3 protein levels were confirmed in absence of inflammatory stimuli and in cells treated with IL-1β (p ≤ 0.034). Our results suggest a novel role of FABP5 protein in AAK progression by controlling expression levels of genes and proteins involved in LEC differentiation. In addition, under inflammatory conditions, FABP5 deficiency affects key transcription factors (PAX6, FOSL2), genes regulating LEC migration, differentiation and cell maintenance (KRT3, VEGFα, MAPK3, CRABP2), and genes involved in inflammation (IL-6, PTGES2). - Source: PubMed
Publication date: 2026/04/28
Amini MaryamHsu Shao-LunStachon TanjaLi ZhenChai NingFries Fabian NSeitz BertholdKundu SwarnaliSuiwal ShwetaSzentmáry Nóra - Systemic sclerosis (SSc) is characterized by fibrosis and vasculopathy affecting the skin and internal organs, leading to multiorgan dysfunction. Injury of microvascular endothelial cells (ECs) in SSc impairs blood flow and causes tissue ischemia, leading to vascular complications such as Raynaud's, digital ulcers, and pulmonary hypertension (PH). PH in SSc presents as group 1 pulmonary arterial hypertension or as group 3 PH related to hypoxia and interstitial lung disease (ILD), both major causes of mortality. Analysis of multiome data from SSc ILD-PH lungs inferred transcription factors regulating EC phenotype, including FOSL2. Overexpression of FOSL2 in transgenic mice (Fosl2tg) leads to vascular changes mirroring human SSc-PH, such as intimal thickening and fibrosis. scRNA-Seq analysis of altered EC gene expression in Fosl2tg mice showed strong overlap with altered EC gene expression in SSc-ILD-PH. Overlapping as well as discrete EC gene expression in Sugen/hypoxia- and hypoxia-treated mice suggested that FOSL2 regulates both hypoxia-dependent and -independent pathways in Fosl2tg mice and SSc-ILD-PH. A deep learning model, ChromBPNet, inferred increased AP-1 binding at base pair resolution in SSc-ILD-PH ECs, and binding to the same motifs was found upon FOSL2 overexpression in primary vascular ECs, highlighting FOSL2's key role in driving the pathological changes seen in SSc-ILD-PH. - Source: PubMed
Publication date: 2026/04/22
Behera RithikaZhou YuechenGerges Peter HFan JingyuTabib TracyGaydosik Alyxzandria MHuang MengqiDas JishnuPachera ElenaHukara AmelaTang YingRenoux FlorianTai MirandaDistler OliverKania GabrielaChan Stephen YSingh HarinderValenzi EleanorLafyatis Robert - A major technical challenge in single-cell transcriptomics is the absence of an integrative analytic pipeline that can simultaneously leverage gene regulatory network (GRN) architecture, AI-assisted gene panel discovery, and functional relevance analyses to generate coherent biological insights. Existing approaches often treat these components independently, focusing on clusters, marker genes, or predictive features without integrating them into a mechanistically grounded framework. Consequently, comprehensive screening that links regulatory association, gene signature screening, and functional interpretation within single-cell datasets remains limited, underscoring the need for an integrated strategy. - Source: PubMed
Publication date: 2026/04/06
Borra SantoshiYan DaWelner Robert SYue Zongliang - The N6-methyladenosine (mA) reader YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) plays a critical role in the tumorigenesis of intrahepatic cholangiocarcinoma (ICC), but its function in the tumor immune microenvironment remains unclear. RNA sequencing analysis of human ICC samples revealed that, among mA-related regulators, YTHDF1 exhibited the most significant negative correlation with immune score. In multiple ICC mouse models, Ythdf1 overexpression enhanced the recruitment of myeloid-derived suppressor cells (MDSCs) and suppressed cytotoxic CD8 T cell responses, promoting ICC progression. Immunostaining of human ICC tissue microarray verified that high YTHDF1 protein expression was significantly associated with increased accumulation of MDSCs and decreased infiltration of CD8 T cells. Mechanistically, YTHDF1 bound to the mA site of FOSL2 mRNA and promoted the translation of FOSL2, a transcription factor driving cytokine CXCL6 expression. Consequently, elevated CXCL6 recruited and activated MDSCs by binding to its receptor CXCR2, leading to the dysfunction of CD8 T cells in ICCs. In addition, targeting YTHDF1 alongside blockade of its downstream chemokine pathway enhanced the efficacy of anti-PD-L1 treatment in preclinical ICC mouse models, serving a promising strategy for improving immunotherapy efficacy in ICC. - Source: PubMed
Publication date: 2026/04/13
Luo LiLiu ZiqinSong ZiminZhang DongLiang CongFang FeiLei KaiWang LinaChen WeikangShen ShunliKuang MingLi XiaoxingYu JunWang ShiyanXu Lixia - Spontaneous abortion (SA) is closely associated with immune homeostasis of decidual natural killer (dNK) cells at the maternal-fetal interface, yet how decidual stromal cells (DSCs) educate NK cells remains incompletely understood. Here, we showed that DSC-derived hyaluronic acid (HA) shapes NK cell residency and cytotoxicity in early pregnancy. - Source: PubMed
Publication date: 2026/03/25
Wang DiZhu JiaweiWang QingzhiShi LingyunHe YehuaJin ZiliChen WenjunChen XiaocongChen ShenjunLi HongZhang CeZhu Rui