Guinea pig Interleukin 1 Delta ELISA kit
- Known as:
- Guinea pig Interleukin 1 Delta Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e05f0089
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Guinea pig Interleukin 1 Delta ELISA kit
Related genes to: Guinea pig Interleukin 1 Delta ELISA kit
- Gene:
- DLK1 NIH gene
- Name:
- delta like non-canonical Notch ligand 1
- Previous symbol:
- -
- Synonyms:
- FA1, pG2, Pref-1, ZOG, Delta1
- Chromosome:
- 14q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-09
- Date modifiied:
- 2019-04-23
Related products to: Guinea pig Interleukin 1 Delta ELISA kit
Related articles to: Guinea pig Interleukin 1 Delta ELISA kit
- Pediatric central precocious puberty (CPP) is driven by premature activation of the hypothalamic-pituitary-gonadal (HPG) axis, along with immune-inflammatory imbalance, metabolic dysfunction, obesity, and gut microbiota-derived signals. According to traditional Chinese medicine (TCM) principles, kidney yin deficiency with hyperactive ministerial fire and spleen deficiency with phlegm-dampness form the basis for central pubertal activation and peripheral metabolic-inflammatory burden, thus supporting a combined approach for obesity-related or mixed-pattern CPP. Representative prescriptions include modified Zhibai Dihuang pills with Liujunzi decoction and modified Danzhi Xiaoyao powder with Erchen decoction, which integrate kidney yin-nourishment and ministerial fire-clearance with spleen qi-strengthening and phlegm resolution. Available clinical evidence suggests potential benefits in controlling secondary sexual characteristics, reducing gonadotropin and sex-steroid levels, and slowing bone-age advancement. Mechanistic studies indicate possible regulation of kisspeptin/GPR54/GnRH and LH/FSH-sex-steroid signaling, Th1/Th2/Treg homeostasis, NF-κB/NLRP3 pathways, adipokine imbalance, insulin resistance, hypothalamic inflammation, and gut microbiota-associated metabolism. However, most mechanistic links remain indirect, comparative trials are scarce, and direct correction of pathogenic MKRN3 or DLK1 variants has not been demonstrated. In this review, we have discussed the role of kidney and spleen dysfunction in CPP and explored the underlying mechanisms - particularly in the context of the neuro-endocrine-immune network that links central neuroendocrine activation with peripheral immune-metabolic signals. In addition, the application of TCM in the management of CPP, and the translational challenges of applying TCM as an adjunct to established CPP management have also been explored. Future research should prioritize CPP-specific pathway validation, identification of syndrome biomarkers, multi-omics-based stratification, multicenter trials, and long-term pediatric safety monitoring. - Source: PubMed
Publication date: 2026/08/25
Luo YujunHuang ChaojieLu YantingHe JieyingChen HailingYang Jinghua - Genomic imprinting secures parent-specific gene expression through differential DNA methylation at imprinted control regions (ICRs). However, how unmethylated alleles resist de novo methylation remains unclear. Using an allelic Dlk1-Dio3 ICR methylation reporter and genome-wide loss-of-function screening, we identify the zinc finger protein GZF1 that binds the unmethylated maternal ICR and protects it from de novo methylation via a regulatory element containing GZF1 and ZFP57 motifs that mediates mutually exclusive, methylation-dependent binding. Loss of either factor causes reciprocal imprinting failure: Gzf1 loss induces maternal allele methylation, H3K4me3 depletion, and silencing of maternal transcripts, whereas Zfp57 loss results in maternalization. Remarkably, GZF1 protects the unmethylated ICR from de novo methylation in both oocytes and embryos, and its loss leads to perinatal death consistent with paternalization of the maternal allele. Together, our findings establish a reciprocal mechanism that maintains parental epigenetic asymmetry across both imprint establishment and embryonic reprogramming. - Source: PubMed
Publication date: 2026/09/02
Toren ArikHoffman LironMiodownik IrinaMayshar YoavBen-Yair RazOrenbuch Ayelet-HashaharRubinstein HernanLifshitz AviezerStok Ranen RoniWainstein AlexanderSheban DaoudShlush LiranTanay AmosAfek ArielStelzer Yonatan - Genomic imprinting is an epigenetic process causing parent-of-origin specific gene expression. The Dlk1-Dio3 domain is one of the largest imprinted clusters. While DNA methylation at an intergenic CpG-island (IG-CGI) within the imprinting control region (ICR) controls expression from the paternal chromosome, mechanisms regulating the unmethylated maternal chromosome remain unknown. Within the transcriptional regulatory element (IG-TRE) of the ICR, deletions identified a minimal region in vitro exhibiting both silencing and enhancing activity, with SOX2 and ZFP281 contributing to enhancer function on the maternal chromosome. In vivo, however, this deletion did not affect maternal expression in mouse embryos; instead it activated Dlk1 on both parental chromosomes. Combining deletion of this IG-TRE with the lethal IG-CGI deletion rescued lethality in mice by balancing Dlk1 expression, despite persistent maternal gene upregulation. These results demonstrate that loss of expression at this domain is more detrimental than gain, highlighting the importance of in vivo analysis. Identification of active regulatory factors on the unmethylated maternal chromosome challenges the prevailing view that imprinting is primarily a methylation-driven phenomenon, further revealing the sophisticated hierarchical mechanisms governing imprinting control. - Source: PubMed
Publication date: 2026/09/02
Weinberg-Shukron AriellaDearden Frances LMoreno-Barriga AnaNew Lok Ting NickMüller MarcoRancourt Rebecca CEdwards Carol AFerguson-Smith Anne C - Loss-of-function mutations in DLK1, encoding Delta Like Non-Canonical Notch Ligand 1, have been linked to central precocious puberty (CPP) and increased body fat in girls, suggesting a role in the connection between metabolism and reproduction. DLK1 is located in the imprinted region of human chromosome 14, and mice lacking Dlk1 exhibit growth retardation and metabolic changes, phenotypes that overlap with Temple syndrome, an imprinting disorder associated with precocious puberty. However, the mechanisms by which DLK1 influences pubertal timing remain unclear. We investigated pubertal timing in Dlk1 knockout (KO) mice with either global or selective central nervous system (CNS) deletion of Dlk1, compared with control mice. Puberty onset and body weight were assessed, along with potential mediators of pubertal timing, including leptin and kisspeptin. Dlk1KO females reached puberty at the same age as controls, despite lower body weight. Dlk1KO males had delayed preputial separation but, like females, reached puberty at significantly lower body weight. Serum leptin and hypothalamic Socs3 mRNA, a downstream leptin effector, were lower peri-pubertally in Dlk1KO females than in controls. Kiss1 mRNA levels in the mediobasal hypothalamus were significantly lower in Dlk1KO females at puberty onset. Selective Dlk1 deletion in neurons and glial cells did not affect pubertal timing. These findings suggest that peripheral sources of Dlk1 contribute to the metabolic and endocrine regulation of pubertal timing. The absence of Dlk1 appears to alter the metabolic milieu in which puberty occurs, allowing activation of the reproductive axis despite low body weight and reduced hypothalamic kisspeptin expression. - Source: PubMed
Macedo Delanie BPereira Sidney AWang MeijiaoKyeol Han KimCarroll Rona SLatronico Ana ClaudiaAbreu Ana PaulaKaiser Ursula B - Understanding the regulation of hematopoietic stem and progenitor cell (HSPC) fate and translating it into effective culture strategies remains a significant challenge. Asymmetric lysosomal inheritance during HSPC division has been shown to predict variations in daughter cell activity and fate, yet the underlying regulators remain unclear. Through cell-cell communication analysis of bone marrow single-cell sequencing data, we identified the Notch ligand Delta-like protein 1 (DLL1) as a potential regulator in HSPC asymmetric division (ACD). Interactions between DLL1-presenting microparticles (MP-Ds) and HSPCs were observed in addressable microwell arrays, simulating cellular responses to localized niche signals. Long-term single-cell tracking revealed that MP-D interactions polarized HSPC lysosomes toward the contact site, directing division orientation and consequent asymmetric lysosomal inheritance in paired daughter cells. Furthermore, this co-culture system enhanced long-term hematopoietic reconstitution capacity of HSPCs in serial transplantations. Our findings support an association between HSPC ACD and the presentation mode of DLL1 signals, which enhances the ex vivo maintenance of HSPCs. - Source: PubMed
Publication date: 2026/08/27
Wenjing LiYiting FengDongbo HanYanxiao AoChen Michael WNing LiYuhong JinHaiwei LiangWen LiuXiaoyu ZhuYanan Du