CIDE-B (C-Terminus 2) Peptide
- Known as:
- CIDE-B (C-Terminus 2) Peptide
- Catalog number:
- 2319P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CIDE- (C-Terminus 2) Peptide
Related genes to: CIDE-B (C-Terminus 2) Peptide
- Gene:
- CIDEA NIH gene
- Name:
- cell death inducing DFFA like effector a
- Previous symbol:
- -
- Synonyms:
- CIDE-A
- Chromosome:
- 18p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-15
- Date modifiied:
- 2018-10-08
- Gene:
- CIDEC NIH gene
- Name:
- cell death inducing DFFA like effector c
- Previous symbol:
- -
- Synonyms:
- CIDE-3, FLJ20871, Fsp27
- Chromosome:
- 3p25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-26
- Date modifiied:
- 2016-10-05
- Gene:
- CIDECP1 NIH gene
- Name:
- cell death inducing DFFA like effector c pseudogene 1
- Previous symbol:
- CIDECP
- Synonyms:
- CICE
- Chromosome:
- 3p25.3
- Locus Type:
- pseudogene
- Date approved:
- 2007-07-26
- Date modifiied:
- 2018-10-08
Related products to: CIDE-B (C-Terminus 2) Peptide
Related articles to: CIDE-B (C-Terminus 2) Peptide
- Obesity poses a significant risk for metabolic disorders, such as insulin resistance and metabolic-associated fatty liver disease (MAFLD), yet effective treatments remain limited. Cell Death-Inducing DNA Fragmentation Factor-α-Like Effector C (CIDEC), a lipid droplet membrane protein, facilitates lipid droplet fusion and is crucial for adipose tissue expansion, making it a key target for obesity and related metabolic diseases. However, previous research revealed that complete genetic deletion of Cidec in adipose tissues, while reducing fat accumulation, induced severe insulin resistance in high-fat diet (HFD)-fed mice, potentially due to ectopic fat storage in the liver. Given that complete knockout is an extreme approach, partial inhibition holds greater clinical relevance. Therefore, this study aimed to investigate the effects of partial inhibition of CIDEC in adipose tissues on fat accumulation and insulin sensitivity in mice. Using the Cre-LoxP system, we generated adipose Cidec haploinsufficient mice. Under a standard diet, these mice exhibited normal body weight, fat accumulation, and insulin sensitivity. Notably, under HFD conditions, mice with partial Cidec deficiency showed reduced fat accumulation in adipose tissues while hepatic fat accumulation remained unchanged, accompanied by improved insulin sensitivity and increased energy expenditure. Mechanistically, we found partial Cidec deficiency activated thermogenic program in adipocytes in vivo and in vitro through the ATGL-PPARα pathway. In conclusion, adipose CIDEC partial inhibition attenuates HFD-induced obesity and insulin resistance by enhancing ATGL-PPARα-mediated energy expenditure, establishing this approach as a promising therapeutic strategy for obesity and related metabolic diseases. - Source: PubMed
Publication date: 2025/07/07
Fu QinghuaWang PengLi WeilinCai ZhenhuaZhao ShijiLing WeidongLi MingxunTang XiaochuanSong Ziyi - The cell death-inducing DFF45-like effector (CIDE) family comprises CIDEA, CIDEB, and CIDEC (fat-specific protein of 27 kDa), all of which are lipid droplet-associated proteins and contribute to fat storage and energy homeostasis. However, the relative impacts of these isoforms on fat storage in adipose tissue and obesity in humans have been unclear. We here examined the expression of CIDE family genes in visceral adipose tissue (VAT) of obese individuals who underwent laparoscopic sleeve gastrectomy and explored its relation to adiposity-related parameters. RNA-sequencing analysis revealed that and were highly expressed in VAT, whereas was expressed at a substantially lower level. and expression levels were positively correlated with body fat mass and subcutaneous adipose tissue (SAT) area, whereas expression was negatively correlated with these markers. In addition, and expression levels showed positive and negative correlations, respectively, with BMI. Multivariable regression analysis showed that only expression was significantly associated with body fat mass. Stratification of the subjects according to tertiles of expression revealed that BMI, body fat mass, and SAT area were significantly greater in the highest expression group than in the other two groups. Our findings thus suggest that, among CIDE isoforms, CIDEC is the most closely associated with fat storage in human adipose tissue. - Source: PubMed
Publication date: 2025/04/08
Iwahashi YasuyukiNishikage SeijiHosokawa YuseiYamada TomokoNakagawa YasushiHirota YushiSakaguchi KazuhikoNishimoto YukiNakajima ShinsukeKitahama SeiichiYamamoto YasuyoshiMukai TomoichiroOgawa WataruTamori Yoshikazu - The cell death-inducing DNA fragmentation factor alpha (DFFA)-like effectors (CIDEs), including CIDEA, CIDEB and CIDEC, regulate the number and size of lipid droplets (LDs) in vertebrates. However, no homologue of CIDE has been reported in plants. Here, we expressed the coding sequences of CIDEA, CIDEB and CIDEC from Mus musculus in tobacco leaves and Brassica napus seeds. The results showed that the size and number of LDs in transiently transformed tobacco leaves were 2.8-3.1 times larger and 24-25 fold more numerous compared to mock-infiltrated leaves, respectively. The total fatty acid (FA) content in CIDE-expressing leaves was increased by more than 50%, and the triacylglycerol (TAG) content was increased by 2-3 fold compared to that of mock-infiltrated leaves. In B. napus seeds, the number of LDs was significantly decreased while the size of LDs was greatly enlarged in CIDE-expressing lines, and the TAG was increased by 10.5%-15.3%. However, the contents of phosphatidylcholine (PC), phosphatidic acid (PA), and phosphatidylserine (PS) were significantly reduced. Almost all metabolites in the glycolytic pathway and some metabolites in the tricarboxylic acid (TCA) cycle were higher in CIDE-expressing seeds compared with WT, and the transcript levels of the related genes were significantly higher than those in WT. The results suggest that the expression of mammalian CIDEs can alter the morphology of LDs and increase oil content in different plant tissues. By enhancing the seed oil content in B. napus, our results offer a new biotechnology strategy to improve oil yield. - Source: PubMed
Publication date: 2025/06/09
Xiong YaoSun CaiyiXiang YuyanLi YuqingGuo LiangLu Shaoping - Obesity is a chronic disease associated with increased risk of cardiovascular disease, diabetes, metabolic dysfunction associated steatotic liver disease and certain cancers. High intensity interval training (HIIT) and moderate intensity continuous training (MICT) are effective in preventing and managing obesity. However, the comparative effects of these modalities on metabolic disorders need to be better mechanistically explored. This study aimed to comprehensively assess the effects of MICT and HIIT on key metabolic organs and underlying mechanisms. C57BL/6 mice were randomized to receive either a chow diet or high fat diet for 12 weeks, followed by random assignment of high-fat-fed mice to no exercise, MICT or HIIT groups for additional 5 weeks. At the end, both HIIT and MICT significantly alleviated high-fat-induced weight gain and lipids disorder and impaired liver function. HIIT was more effective in enhancing insulin sensitivity, ameliorating hepatic steatosis, reducing adipocyte hypertrophy. Additionally, HIIT restored the high-fat-induced downregulation of Cidea, Cidec and Atgl in inguinal white adipose tissue and liver. Furthermore, HIIT resulted in upregulation of interleukin 6 (Il-6) in skeletal muscle. The exogenous addition of Il-6 to primary white adipocytes significantly downregulated Cidec, and up-regulated Atgl expression. In conclusion, HIIT is superior to MICT in improving metabolic dysfunction, likely mediated through Il-6-induced downregulation of Cidea and Cidec, thereby promoting lipolysis. - Source: PubMed
Publication date: 2025/04/30
Lu XiChen YonglianXie QingxingTong Nanwei - High fat diet (HFD) induces the enlargement and accumulation of lipid droplets (LDs) in hepatocytes, thereby influencing the homeostasis of lipid metabolism. Cell death-inducing DNA fragmentation factor-α-like effector C (CIDEC), a surface protein of LDs, facilitates their fusion and growth, transforming small LDs into larger ones. Lipophagy, a selective form of autophagy, primarily targets small LDs for degradation. Fisetin (FIS), a natural dietary flavonoid present in various fruits and vegetables, has an unclear mechanism for reducing LD accumulation. In this study, we observed that FIS significantly ameliorated HFD-induced lipid accumulation in the hepatocytes of C57BL/6 mice. In further mechanistic studies, we revealed that FFA enhanced the expression of CIDEC, which promoted the fusion of LDs and caused them to become larger. The enlarged LDs could not be degraded by autophagy, which ultimately led to accumulation of LDs. Conversely, FIS alleviated LD accumulation by inhibiting CIDEC-mediated fusion, resulting in smaller LDs that facilitated lipophagy. Additionally, studies indicated that the dysfunction of circadian rhythms is closely related to lipid metabolism. In our study, we showed that HFD and FFA disrupted circadian rhythm in C57BL/6 mouse hepatocytes and AML12 cells, while FIS modified the rhythm disturbances and increased protein expression of the core clocks BMAL1 and CLOCK. We silenced the BMAL1 protein and revealed that si-BMAL1 upregulated CIDEC proteins. These data suggested that FIS might inhibit CIDEC-mediated LD fusion and enhance hepatocyte lipophagy by promoting the expression of rhythm protein BMAL1, thereby alleviating LD accumulation in C57BL/6 and AML12 cells caused by the HFD and FFA. The present study provided novel insights and potential targets for utilizing functional food factors to mitigate the accumulation of LD in hepatocytes. - Source: PubMed
Publication date: 2024/11/20
Zhang RanranLiu MeitongLu JingLu ShujingWang YuanmengGuan Shuang