LASS1 Blocking Peptide
- Known as:
- LASS1 Blocking Peptide
- Catalog number:
- 33r-5564
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- LASS1 Blocking Peptide
Related genes to: LASS1 Blocking Peptide
- Gene:
- CERS1 NIH gene
- Name:
- ceramide synthase 1
- Previous symbol:
- LASS1
- Synonyms:
- LAG1, UOG1
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-14
- Date modifiied:
- 2016-10-24
Related products to: LASS1 Blocking Peptide
Related articles to: LASS1 Blocking Peptide
- Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS), a common sleep-related breathing disorder, is closely associated with an increased risk of cardiovascular and metabolic comorbidities. Polysomnography, the diagnostic gold standard, is costly and environmentally sensitive. This study explored the diagnostic potential of miR-1180-3p and its role in Chronic Intermittent Hypoxia (CIH)-induced vascular injury. - Source: PubMed
Publication date: 2026/04/23
Deng MulanChen YanjieChen HongyeChen Qihui - Sirtuin 1 (Sirt1), a member of the sirtuin family, is integral to the regulation of energy homeostasis, cellular metabolism, and stress responses. While Sirt1 has been intensively studied in mammals, studies on this gene in aquatic animals, especially turbot, is relatively limited. In this study, the sirt1 gene was cloned. The open reading frame (ORF) of the Sirt1 consists of 2187 base pairs, encoding a 728-amino-acid protein that contains a SIR2 domain. Compared with the siRNA-NC group, Sirt1 knockdown resulted in a significant downregulation of mRNA expression levels of the tight junction proteins occludin, tricellulin, claudin3, and zo1, as well as protein levels of Occludin and ZO1, within the intestinal tissue of turbot. Concurrently, it markedly inhibited the expression of genes associated with ceramide synthesis (sptlc2, kdsr, cers1, cers2, cers3, smpdl3a, smpdl3b, neu1, glb1, gba1, and sgpp2) and ceramide catabolism (sgms1a, ugcg, b4galt, and sphk1) in the same tissue. Conversely, compared to the pcDNA3.1 group, Sirt1 overexpression significantly enhanced the mRNA expression levels of occludin, tricellulin, claudin3, claudin7, and zo1, along with the protein level of Occludin. Furthermore, Sirt1 overexpression significantly elevated the expression of genes involved in ceramide synthesis (cers2, cers3, smpd3, smpdl3b, neu1, glb1, gba1, sgpp2) and ceramide catabolism (sgms1a, galt, b4galt, and sphk1). These results suggest that Sirt1 may influence the intestinal mechanical barrier by acting on the metabolic balance of ceramide and altering the expression of intestinal tight junction proteins, thus playing a crucial role in maintaining the intestinal health of turbot. - Source: PubMed
Publication date: 2026/03/18
Ma XiuhuaLiu QianhuiMai KangsenZhang Yanjiao - Autism spectrum disorder (ASD) is a heterogeneous neurological condition with an unclear etiology and pathogenesis. In recent years, studies have identified changes in lipid metabolism, inflammation, mitochondrial dysfunction, and mitophagy in patients with ASD. However, the specific interactions between these molecular signatures and their clinical applications in ASD remain largely unexplored. The aim of our study is to search for correlations between changes in gene and miRNA expression and the clinical characteristics of ASD. The investigation included a cohort of children with idiopathic ASD and healthy controls (HC). Diagnosis was established based on ADOS assessment (autism diagnostic observation schedule). Gene expression levels of sphingomyelin phosphodiesterases (SMPD1 and 5), ceramide synthases (CerS1 and 6), cyclooxygenase-2 (COX2), chitinase-3-like protein 1 (YKL40), and lysosome-associated membrane proteins 1 and 2 (LAMP1 and 2) were assessed using qPCR. The TaqMan assay was used for the quantification of miR-143-3p and miR-181a-5p. Our findings provide novel data on altered expression profiles of molecules related to lipid metabolism and LAMP1/2 in patients with ASD. We observed increased mRNA levels of CerS1, SMPD5, COX2, YKL40, LAMP1, and LAMP2 and decreased expression of miRNA-181a-5p in ASD patients compared to HC. Additionally, we identified a correlation between CerS1, CerS6, COX2, and miRNA-143-5p with ADOS scores. Multiple regression analysis revealed that 48.0% of the variance in the total ADOS score was explained by the combined effects of COX2, miRNA-143-3p, CerS1, CerS6 and age. These results provide new insights into the molecular alterations associated with ASD and may reinforce future studies aimed at clarifying their functional relevance. - Source: PubMed
Publication date: 2026/02/14
Gevezova MariaMaes MichaelPacheva IlianaMehterov NikolayIvanov ZdravkoTimova ElenaSpassieva StefkaBieberich ErhardKazakova MariaIvanov IvanSarafian Victoria - PEL is an aggressive B-cell lymphoma that in the majority of cells harbors latent KSHV, although appropriate stimuli can induce viral replication. These include HDAC inhibitors such as butyrate, activation of endoplasmic reticulum (ER)/UPR stress, and exogenous administration of ceramide 18. These treatments reduce cell survival, but also activate adaptive branches of the UPR such as the Ire1α-XBP1s axis and/or trigger macroautophagy to counteract cell death, processes whose output may be manipulated by KSHV. HSPs are also upregulated by several cytotoxic treatments and support both cell survival and KSHV replication, suggesting a complex relationship between cell and viral fate. In this study, we demonstrate that HSP27 inhibition reduces PEL cell survival, activates ER stress including XBP1s, and upregulates CerS1, the enzyme that synthesizes ceramide 18. We further discovered a crosstalk between XBP1s and CerS1 that enhances protection against ER stress during HSP27 inhibition also promoting DRP1-dependent pro-survival mitophagy and triggers KSHV reactivation from latency. In conclusion this study suggests that HSP27 plays a previously unrecognized central role in controlling the UPR, CerS1 and mitochondrial autophagy, influencing both cell survival and KSHV lytic cycle in PEL cells. - Source: PubMed
Publication date: 2026/02/26
Gonnella RobertaCorrado VincenzoScaffidi Giulio FrancescoBenedetti RossellaDi Crosta MicheleZarrella RobertaGilardini Montani Maria SaveriaSantarelli RobertaCirone Mara - Hepatocellular carcinoma (HCC), which makes up about 90% of liver cancer, is the third leading cause of cancer-related death. Recent studies suggest that metabolites derived from the gut microbiome may offer new therapeutic opportunities for HCC. In this study, we explored whether microbial metabolites could enhance the effectiveness of sorafenib, a first-line multi-kinase inhibitor used in advanced HCC. Through a screen of a microbiome metabolite library, we identified spermine and sphingosine as potential candidates that boosted anticancer effects of sorafenib in HepG2, Huh7, and SK-Hep-1 cells. These metabolites worked synergistically with sorafenib to suppress tumor growth in cultured HCC cells, patients-derived HCC organoids, and a xenograft mouse model. Mechanistically, spermine triggered cell cycle arrest at the S phase, while sphingosine and sorafenib induced G1 arrest, contributing to an increased sub-G1 population and apoptosis when combined. Notably, sorafenib treatment led to the downregulation of (a key catabolic enzyme for spermine), as well as and (critical enzymes involved in sphingosine metabolism), whose high expression levels are associated with poorer survival outcomes in liver cancer patients according to TCGA data. A 16S rRNA sequencing analysis revealed that combination of sorafenib with spermine or sphingosine alters the gut microbiome, increasing the relative abundance of inversely correlated with tumor sizes in a xenograft mouse model. Therefore, we propose that combining sorafenib with spermine or sphingosine could enhance its anti-HCC effects by promoting apoptosis and reducing the expression of metabolic enzymes. Moreover, may serve as a potential microbiome-based prognostic marker for HCC. - Source: PubMed
Publication date: 2026/01/01
Jang Hay-RanKim Hyun-JinKim Bo-YoungJeong Jae-HoonKim Jeon-KyungWon Jin AhYoo Hye HyunLee Yong GuYim Hyungshin