Human Interleukin 1 Delta (IL1d)ELISA Kit
- Known as:
- Human Interleukin 1 Delta (IL1d)Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-2762
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Interleukin 1 Delta (IL1d)ELISA Kit
Related genes to: Human Interleukin 1 Delta (IL1d)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: Human Interleukin 1 Delta (IL1d)ELISA Kit
Related articles to: Human Interleukin 1 Delta (IL1d)ELISA Kit
- is a paternally expressed gene encoding a transmembrane protein belonging to the Delta-Notch signaling family, increasingly recognized for its role in fetal growth regulation. This study explores the relationship between genetic variants (SNV) and birth weight and the potential sex-specific differences in this association. This cross-sectional study consists of a sample of 949 participants (499 males and 450 females) with available birth weight information obtained from official birth certificates. Five SNVs located within or near the gene (rs1802710, rs876374, rs7155375, rs57098752, and rs7149242) were genotyped using Real-Time PCR with predesigned TaqMan™ Assays. Three SNVs (rs1802710, rs876374 and rs7149242) were significantly associated with birth weight in males, but not in females. Interestingly, heterozygous males had a higher mean birth weight than homozygous males. Further confirming this association, heterozygotes for these SNVs were more frequent among males with birth weight above the population mean (3.4 kg) compared to those below it. variants are associated with birth weight in a sex-dependent manner and with an inheritance pattern compatible with polar overdominance. This places as a genetic factor to be considered when evaluating health conditions related to higher or lower than normal birth weight. - Source: PubMed
Publication date: 2026/06/18
Pomares OlgaPérez-Nadador IrisMejorado-Molano Francisco JParra-Rodríguez AlejandroSoriano-Guillén LeandroLaborda JorgeGarcés Carmen - Despite improved treatment options for triple-negative breast cancer (TNBC) patients including immune checkpoint blockade (ICB) alongside chemotherapy, clinical prognosis for these individuals remains poor with regard to disease recurrence and tumor metastasis. Novel interventional approaches are desperately needed. A promising immunotherapeutic strategy involves the selective targeting of tumor blood vessels to coordinately limit tumor growth and metastasis. Here, we describe the use of a dendritic cell (DC) vaccine to elicit immunity against the conserved tumor blood vessel antigen (TBVA) DLK1, which is upregulated and expressed by abluminal pericytes in the tumor microenvironment (TME) of TNBC patients. Our results demonstrate the ability of therapeutic DC vaccination to safely provoke anti-angiogenic T cell activation and recruitment into the TME, resulting in significant reduction in primary and metastatic tumor burden in translational TNBC mouse models when co-administered with anti-PD1 ICB. Interestingly, vaccines targeting DLK1 also promote spreading of polyclonal T cell responses against TNBC antigens that likely fortified tumor control in treated mice. These findings support the anti-tumor efficacy of DC-based vaccines targeting DLK1 and the translation of this approach as a novel treatment strategy for patients with TNBC. - Source: PubMed
Publication date: 2026/06/23
Daugherity Elizabeth ALawrence CarynOkpalanwaka Izuchukwu FMouw TylerArif DauodAppiah DukeStorkus Walter JLowe Devin B - Activating anaplastic lymphoma kinase () mutations define a clinically relevant subset of neuroblastoma (NB), yet -linked transcriptional programs with robust prognostic value remain insufficiently characterized. This study aimed to identify -associated transcriptional features across single-cell and bulk datasets and to develop a reproducible prognostic signature for NB. - Source: PubMed
Publication date: 2026/04/24
Zhu AiguoXia YurenLi XinJin ZhengchaoWang JianPan Yi - Genomic imprinting, an epigenetic mechanism that governs parent-of-origin-specific gene expression, is essential for mammalian development, yet its role in late-stage development remains unclear due to the lethality of parthenogenetic (Pg) embryos. Here, we establish cell replacement with parthenogenote-derived cells (CReP), a blastocyst complementation strategy that enables survival and tissue-specific contribution of Pg-derived cells. By creating tissue-specific niches in recipient embryos, CReP allows targeted incorporation of Pg-derived cells into late-stage tissues. Brain-targeted CReP showed that Pg-derived cells can participate in neural development but exhibit impaired maintenance of neuronal-glial balance, accompanied by increased Notch signaling and reduced expression of the paternally expressed gene Dlk1. Recombinant Dlk1 attenuated Notch activity and shifted neuronal differentiation toward control levels. These findings support a key contribution of the paternal genome to neural stem cell expansion and balanced cell fate decisions, in part through Dlk1-Notch-related pathways. The CReP model provides a powerful platform for investigating genomic imprinting and parental genome contributions in development and disease. - Source: PubMed
Publication date: 2026/06/08
Takechi MarinaZhu YezhangLu ZezhenZeng YingMizutani Ken-IchiNakano ToruShen LiYamaguchi Shinpei - Vascular dementia (VaD) is characterized by chronic cerebral hypoperfusion, leading to cognitive decline. Impaired hippocampal neurogenesis is a crucial pathological feature of VaD. Delta-like 1 homolog (Dlk1)-Notch signaling may contribute to neural stem cell regulation, but the involvement of Dlk1-Notch signaling in impaired hippocampal neurogenesis during hypoperfusion is unclear. Here, we investigated the role of Dlk1 and Notch signaling in a mouse model of chronic cerebral hypoperfusion induced by bilateral carotid artery stenosis (BCAS). We found that BCAS increased Dlk1 levels in hippocampal tissue and cerebrospinal fluid, accompanied by elevated Notch intracellular domain (NICD) expression and reduced doublecortin (Dcx)-positive hippocampal cells. These changes were associated with impaired novel object recognition. In Neuro2a cells, hypoxia-mimetic treatment elevated NICD and extracellular Dlk1 and reduced cell viability, while pharmacological inhibition of Notch signaling partially rescued cell loss and attenuated these changes. These findings suggest that Dlk1-associated Notch activation correlates with impaired hippocampal neurogenesis and memory dysfunction under chronic hypoperfusion. Our results highlight a potential link between altered niche signaling and cognitive decline in VaD, providing a basis for further mechanistic investigation. - Source: PubMed
Publication date: 2026/05/28
Moriyama YoshiyukiHasegawa RenaEndo HikaruMatsumura SayakaKaneko RyotaroHayashi HidekiIwatani YuiTakagi Norio