Ask about this productRelated genes to: SIM1 Blocking Peptide
- Gene:
- SIM1 NIH gene
- Name:
- SIM bHLH transcription factor 1
- Previous symbol:
- -
- Synonyms:
- bHLHe14
- Chromosome:
- 6q16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-22
- Date modifiied:
- 2018-04-20
Related products to: SIM1 Blocking Peptide
Related articles to: SIM1 Blocking Peptide
- Rare and deleterious variants in the leptin-melanocortin pathway can underlie severe childhood obesity, but data from East Asian populations remain limited. - Source: PubMed
Publication date: 2026/08/03
Chang Yu-MingHwang Daw-YangChou Yen-YinPan Yu-WenWeng Yun-HanTsai Meng-Che - Obesity is increasingly being recognized as a heterogeneous condition with strong genetic underpinnings. Monogenic obesity, caused by single-gene mutations, primarily affects the leptin-melanocortin pathway, which regulates hunger and satiety. Mutations in genes, such as , , , , and , lead to hyperphagia, early onset severe obesity, and metabolic dysregulation. and mutations impair leptin signaling, resulting in defective appetite suppression, whereas and deficiencies disrupt prohormone processing. mutations, the most common cause of monogenic obesity, impair satiety signaling and are linked to rapid weight gain. Syndromic obesity, including the Bardet-Biedl and Alström syndromes, involves ciliary dysfunction, leading to developmental abnormalities alongside obesity. Other genes such as , , and play crucial roles in hypothalamic development and energy regulation. Advances in genomic sequencing have improved the recognition of genetic etiologies; however, many patients remain undiagnosed due to limited testing availability and a lack of clinician awareness. Precision therapies, including set-melanotide for specific melanocortin pathway defects, demonstrate the promise of targeted treatments. However, management must extend beyond pharmacology; lifestyle interventions, psychosocial support, and family-centered care remain essential, especially when intellectual disability or behavioral challenges complicate adherence. Ethical considerations surrounding access and equity are critical, as high-cost therapies and the limited availability of genetic testing risk widening disparities between health systems. Polygenic risk scores and multi-omics approaches may expand precision medicine beyond rare genetic syndromes to common obesity, highlighting the importance of integrating genetics, psychosocial care, and policy advocacy in the management of pediatric obesity. - Source: PubMed
Publication date: 2026/02/09
Khalil HadelFeigin EugeneZaitoon Hussein - Catheterization of the left gastric artery (LGA) is often challenging due to acute angulations that compromise catheter stability. We describe the Simmons (SIM)-lock technique, a novel approach using a standard 5-Fr SIM-1 catheter and a coaxial microcatheter. The microcatheter is first advanced into a distal branch to serve as an anchor, allowing the SIM1 catheter to be deep-seated within the celiac trunk. Upon removal of the microcatheter, the SIM1 catheter assumes its functional recurved shape, with the tip oriented cranially. A controlled pullback maneuver then causes the free tip to slide and lock securely into the LGA ostium. This method transforms a typically unstable engagement into a controlled, stepwise procedure, providing a stable platform for intervention while utilizing standard, cost-effective equipment. - Source: PubMed
Publication date: 2026/07/17
Sevinç Ömer FarukArık ErbilTaydaş OnurBeşler Muhammed Said - Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of several human cancers, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL), both of which still lack effective treatment options. Members of the bromodomain and extra-terminal domain (BET) family, especially bromodomain-containing protein 4 (BRD4), play important roles in RNA polymerase II-mediated transcriptional regulation and are required for the expression of many tumor-driving oncogenes in various cancer cells. Therefore, BET proteins have become attractive targets for anticancer drug development. Previous studies have demonstrated the high sensitivity of PEL cells to BET inhibitors, and BRD4 silencing effectively blocks tumor cell proliferation. In contrast, KSHV-infected immortalized endothelial cells display strong resistance to BET inhibitors, including (+)-JQ1. To further develop BRD-targeted therapies for KSHV-infected immortalized endothelial cells, we identified MZ-1 and SIM-1, two BRD4 PROTAC degraders, as effective inhibitors of cell growth in these cells. Mechanistically, these inhibitory effects depend on suppression of LANA translation through increased eIF2α phosphorylation in KSHV-infected cells. Similar LANA suppression was also observed following RNAi-mediated silencing of BRD2 or BRD4. Proteomic analysis identified unique protein candidates altered in MZ-1- and SIM-1-treated KSHV-infected immortalized endothelial cells compared with (+)-JQ1-treated cells. In summary, our study develops an effective strategy against KSHV-infected immortalized endothelial cells using selective BRD PROTACs, which may help improve therapeutic outcomes for KSHV-related malignancies in the future. - Source: PubMed
Publication date: 2026/06/01
Chen JungangFan JiaojiaoQin MargaretLin ZhenMu ShengyuDai LuQin Zhiqiang - The amyloid precursor protein (APP) is associated with Alzheimer's disease. Appl is the single Drosophila APP ortholog and is expressed in all neurons throughout development. Appl was previously shown to cell-autonomously modulate axon outgrowth in the mushroom bodies (MBs), the fly olfactory memory center. However, we found that Appld, the only reported null allele, affects the normal function of vnd, the gene just proximal to Appl. To decipher developmental and memory defects specifically due to a loss of only Appl function, we generated a precise Appl null allele (ApplC2.1) by CRISPR/Cas9 genomic engineering. With ApplC2.1, we confirmed the partial contribution for Appl in MB axon outgrowth. We also produced new CRISPR vnd alleles removing either vnd-B or vnd-A function. We report here that vnd is also required for MB β-branch axon outgrowth and to a much greater extent than Appl itself. Moreover, vnd is expressed in neurons close to, but not within, the MB during development and is required non-cell-autonomously for MB axon outgrowth. It was previously shown that Appl knockdown in the MBs results in loss of memory following the association of odorants with electric shocks. Differently from Appld flies we found no defects of electric shock avoidance in ApplC2.1 flies, allowing us to test for memory. ApplC2.1 flies showed a complete loss of long-term memory which was fully rescued by MB-restricted expression of Appl+ only during the adult stage. Therefore, we demonstrate that the complete lack of Appl affects memory independently from structural developmental defects. - Source: PubMed
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