Isl1 EMSA Kit
- Known as:
- Isl1 EMSA Kit
- Catalog number:
- AY1199
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- Isl1 EMSA Kit
Related genes to: Isl1 EMSA Kit
- Gene:
- ISL1 NIH gene
- Name:
- ISL LIM homeobox 1
- Previous symbol:
- -
- Synonyms:
- Isl-1, ISLET1
- Chromosome:
- 5q11.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2016-10-05
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- METTL14 mediates N6-methyladenosine (mA) RNA modification, while YTHDC1 and YTHDF2 specifically bind mA-methylated RNA to regulate RNA fate. POMC neurons constitute the core of the central melanocortin circuit, and POMC deficiency causes obesity in both mice and humans. However, how mA-based epitranscriptomics regulates melanocortin circuit function remains unclear. Here, we generated and characterized POMC neuron-specific knockout mice lacking Mettl14 (Mettl14), Ythdc1 (Ythdc1), or Ythdf2 (Ythdf2 ). Mettl14 and Ythdc1 mice develop hyperphagia, obesity, glucose intolerance, insulin resistance, and hepatic steatosis in both sexes under standard chow conditions, accompanied by POMC downregulation. Conversely, POMC neuron-specific overexpression of METTL14 or YTHDC1 protects against diet-induced obesity. In contrast, Ythdf2 mice are resistant to obesity, revealing an mA-dependent balance between YTHDC1 and YTHDF2. Mechanistically, the METTL14/YTHDC1 pathway is indispensable for embryonic POMC neurogenesis, while in adults YTHDC1 maintains melanocortin circuit integrity/function. METTL14 and YTHDC1 directly target POMC and ISL1 transcripts to regulate protein expression. POMC neuron-specific restoration of POMC reverses obesity and metabolic phenotypes in Mettl14 and Ythdc1 mice, defining an anti-obesity METTL14/mA/YTHDC1/POMC axis. These findings identify METTL14 as the mA writer for POMC/ISL1 and YTHDC1 and YTHDF2 as their readers, uncovering a critical role of mA epitranscriptomic regulation in melanocortin circuit development and maintenance. - Source: PubMed
Publication date: 2026/04/15
Li YuanKim Min-HyunRen DechengRui Liangyou - Early apoptosis of grafted islets is one of the critical challenges that significantly impact the efficacy of islet transplantation. We employed Staurosporine to pre-induce apoptosis in bone marrow mesenchymal stem cells (BMSCs). The conditioned medium from apoptotic BMSCs was then used to pretreat β cells, which notably enhanced the suppression of β cell apoptosis. For in vivo experiments, co-transplantation of islets and apoptotic BMSCs under the renal capsule of diabetic rats inhibited islets apoptosis and resulted in better transplantation outcomes. Subsequently proteomic analysis revealed that the iron-loaded form of Lcn2 protein (holo-Lcn2) secreted by apoptotic BMSCs played a crucial role in exerting anti-apoptotic effects. Holo-Lcn2 binds to the Slc22a17 transporter on cell membrane, facilitating the transport of Fe into cells. Inhibition of Fe transport suppressed the anti-apoptotic effect of holo-Lcn2. Thus, we hypothesize that apoptotic BMSCs reduce grafted islets apoptosis through the holo-Lcn2/Slc22a17/Fe axis. This study provides insights into the application of BMSCs-based acellular therapies in islet transplantation. - Source: PubMed
Publication date: 2026/04/10
Lu CuinanWang JialeWang YingWang JingwenBi HuanjingYu XiaoyangChen ZuhanDong BoqingMa RuiyangDing Xiaoming - Enhancer of zeste homolog 2 (EZH2), the catalytic subunit of Polycomb Repressive Complex 2, catalyses H3K27 trimethylation and directs lineage development programs, yet its function in early multipotent progenitors remains incompletely understood. ISL1 marks cardiopharyngeal and neural crest progenitors that contribute to second heart field derivatives and to craniofacial and limb morphogenesis. Here, Isl1-cre lineage tracing showed that lineage derivatives populated the cardiopharyngeal region and the posteromedial hindlimb bud during mid-gestation, and contributed extensively to the developing right ventricle, outflow tract, and hindlimb. Loss of Ezh2 in Isl1-expressing progenitors resulted in a high incidence of congenital heart defects, dominated by incomplete atrial and ventricular septation and outflow tract malformations, including double outlet right ventricle and persistent truncus arteriosus. These defects were accompanied by ventricular wall thickening at birth. In parallel, Ezh2 mutants exhibited hindlimb skeletal abnormalities, including pelvic and tarsal malformations with impaired ossification. These abnormalities were associated with cyanosis and perinatal demise. Together, these findings identify a requirement for EZH2 in Isl1-lineage contribution to heart and hindlimb development. - Source: PubMed
Publication date: 2026/04/15
Ammar HamnaPatolsky Daniel BChi LijunCaballero Amalia NDelgado-Olguín Paul - Patients with high-risk neuroblastoma (NB) continue to have long-term survival rates below 60%, with relapse occurring in more than half of patients, likely driven by chemoresistant minimal residual disease in the bone marrow (BM-MRD). Although several quantitative PCR (qPCR) and droplet digital PCR (ddPCR) assays measuring different but overlapping sets of NB-associated mRNAs (NB-mRNAs) have shown a significant prognostic value at various time points, the optimal combination of MRD markers (a set of NB-mRNAs) and evaluation timing remains unclear. In the present study, 89 bone marrow samples were collected from mostly overlapping 30 high-risk NB patients at four time points: diagnosis (Dx), end of induction (EOI), end of high-dose chemotherapy (EOH), and end of consolidation (EOC). BM-MRD was assessed with a 7NB-mRNAs ddPCR assay quantifying CRMP1, DBH, DDC, GAP43, ISL1, PHOX2B, and TH mRNAs. BM-MRD at EOH and EOC time points was significantly associated with relapse. Moreover, patients with higher BM-MRD levels at EOH (7NB-mRNAs ≥ 3.5) and EOC (7NB-mRNAs ≥ 3.5) time points had significantly inferior 3-year event-free survival (EOH, = 0.003; EOC, = 0.033). These results indicate that EOH and EOC are clinically informative evaluation time points for BM-MRD detected by 7NB-mRNA expression. - Source: PubMed
Publication date: 2026/03/05
Mon Cho YeeNay Win Kaung HtetNishimura AkihiroNakatani NaokoTamura AkihiroYamamoto NobuyukiNino NanakoUemura SuguruSaito AtsuroIshida ToshiakiMori TakeshiHasegawa DaiichiroOkuno KeisukeKosaka YoshiyukiIshizawa KikyoUmemoto MayunoMatsui TaiseiNagatani AyakaNishimura Noriyuki - It is well known that TGF-β plays a key role in the progression of pulmonary fibrosis. However, how TGF-β/SMAD3 regulates downstream effector genes and its effect on alternative splicing in pulmonary fibrosis is still not fully understood. Here, we established a TGF-β-induced pulmonary fibrosis model in mouse primary fibroblasts to verify the potential role of TGF-β/SMAD signaling in pulmonary fibrosis. In both NIH3T3 and primary fibroblast models of fibrosis, the TNF signaling pathway was significantly enriched among differentially expressed genes, highlighting its core role in driving fibrotic processes. By integrating RNA-seq, CUT&Tag data from fibrotic primary fibroblasts, we found that TGF-β/SMAD3 indirectly regulated the TNF pathway gene Vcam1 through the transcription factor Isl1. Furthermore, using full-length isoform sequencing, we found that fibrosis was associated with a reduction in the number of genome-wide alternative splicing events, particularly in TNF pathway effector genes like Vcam1 and Vegfd. Dual dysregulation of TNF signaling drives fibroblast resistance to apoptosis and aggravates fibrosis. Thus, our study reveals a unique mechanism by which TGF-β/SMAD signaling regulates transcription and coordinates genome-wide alternative splicing to drive pulmonary fibrosis progression. - Source: PubMed
Publication date: 2026/02/27
Wang PeijunGuo MingliangZhang ZhengxuanLiu GuojunLiu ChunchengCai LuZhao Hongyu