IL6 & ZBTB16 Protein Protein Interaction Antibody Pair
- Known as:
- IL6 & ZBTB16 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0512
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- IL6 & ZBTB16 Protein Interaction Antibody Pair
Related genes to: IL6 & ZBTB16 Protein Protein Interaction Antibody Pair
- Gene:
- ZBTB16 NIH gene
- Name:
- zinc finger and BTB domain containing 16
- Previous symbol:
- ZNF145
- Synonyms:
- PLZF
- Chromosome:
- 11q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-01
- Date modifiied:
- 2016-10-05
Related products to: IL6 & ZBTB16 Protein Protein Interaction Antibody Pair
Related articles to: IL6 & ZBTB16 Protein Protein Interaction Antibody Pair
- Geographic variability in the clinical efficacy of tonsillectomy for immunoglobulin A nephropathy (IgAN) suggests population-level differences in mucosal immune architecture. However, the molecular features of the tonsillar germinal center (GC) microenvironment-the central site for IgA class switching and mucosal B-cell activation-remain poorly characterized, particularly in relation to glomerular injury severity. - Source: PubMed
Publication date: 2026/05/22
Kawabe MayukoYamamoto IzumiOhki YutaroHayashi AyakaKanzaki GoMatsumoto KeiUeda HiroyukiHirano KeitaTsuboi NobuoYokoo Takashi - Multiple sclerosis (MS) is a complex immune-mediated disorder with polygenic and multicellular underpinnings, necessitating cell-type-specific molecular studies to delineate dysregulated pathways. Here, we profile 1,075 transcriptomes from 167 patients with MS and 42 healthy participants across six peripheral immune cell-type-states. MS-associated transcriptional differences are more pronounced in primary (unstimulated) immune cells than in in vitro-stimulated counterparts. We identify shared and cell-type-specific transcriptional alterations at the level of genes, pathways, and co-expressed gene modules, prioritizing regulators, such as ZBTB16, across T cells and monocytes, and replicating six MS-associated modules in independent datasets. The top T cell module is enriched for MS susceptibility genes and affects proliferation. The top monocyte module implicates dysregulated TNF-α/NF-κB signaling, for which an in silico drug screen and in vitro validation nominate alvespimycin as a candidate modulator. Together, these findings define stable peripheral immune dysregulation signatures in MS that may serve as diagnostic or prognostic biomarkers in at-risk individuals. - Source: PubMed
Publication date: 2026/06/05
Roostaei TinaFujita MasashiTouil HananeKivisäkk PiaMcCabe CristinNejad ParhamSabrin AfsanaGarcia Frankie Gvan Dorp Christiaan HFelsky DanielVlachos Ioannis SHui DanielFransson JenniferMacnair WillWilliams AnnaZhang LiliZhu WenXia ZongqiZujovic ViolettaPatsopoulos Nikolaos AYates Andrew JKuchroo Vijay KChitnis TanujaWeiner Howard LKlein Hans-UlrichDe Jager Philip L - Mucosal-associated invariant T (MAIT) cells are innate-like T lymphocytes involved in immune surveillance and tissue homeostasis. Yet, their transcriptional dynamics and functional crosstalk with macrophages at the time of myocardial injury are incompletely defined. - Source: PubMed
Publication date: 2026/05/20
Kang HaofeiWang JunjieRuan RenjieWen YudanChen BingruWu MeixiangWang YongguangZhang Yunrui - Zinc finger and BTB domain‑containing protein 16 (ZBTB16) plays diverse roles in a number of different cancer types, but its function and mechanism in esophageal cancer remain ambiguous. The present study was, to the best of our knowledge, the first demonstration that ZBTB16 was highly expressed in esophageal cancer tissues and cell lines. Knockdown of ZBTB16 significantly inhibited the proliferation and migration of esophageal cancer cells. Furthermore, ZBTB16 silencing increased the rate of cell death in esophageal cancer cells and induced mitochondrial membrane potential loss, intracellular copper accumulation and elevated oxidative stress. Mechanistically, knockdown of ZBTB16 downregulated the expression of ATPase copper‑transporting α and ATPase copper‑transporting β (ATP7B), while upregulating copper uptake protein 1 and ferredoxin. The present study further demonstrated that ZBTB16 knockdown increased the production of reactive oxygen species, which was partially rescued by ATP7B overexpression. In a mouse xenograft model of esophageal cancer, ZBTB16 knockdown markedly suppressed tumor growth, significantly reduced tumor weight and volume and notably altered the expression of cuproptosis‑related proteins . Summarily, ZBTB16 promoted the development of esophageal cancer by regulating copper homeostasis and oxidative stress. Therefore, ZBTB16 may represent a potential therapeutic target for the treatment of esophageal cancer. - Source: PubMed
Publication date: 2026/05/22
Wang JingyiYang BinPeng ShengzuYang Bin - Dexamethasone (DEX) is used in clinical practice as a life-saving therapy in threatened preterm birth; however, such treatment also represents a powerful signal that can reprogram fetal physiology, including the circadian system. The effect of DEX on the fetal circadian clock in the suprachiasmatic nuclei (SCN) has been demonstrated, but the underlying mechanism has been unaddressed. The aim of this study was to provide insight into the DEX-induced transcriptional effects in the fetal SCN of mPer2 mice. We used triple-labeled immunofluorescence to localize glucocorticoid receptors (GR) in the fetal SCN, cultured ex vivo fetal SCN explants to monitor PER2-driven bioluminescence (PER2::LUC) rhythms, and RNA-seq and RT qPCR analyses to identify genes differentially expressed after DEX and vehicle treatments. We demonstrate that GRs are homogenously expressed in all cells (neuronal and glial nuclei and glial processes) of the fetal SCN. Monitoring PER2::LUC in fetal SCN explants confirmed that most cells respond to DEX with increased amplitude and mesor of the rhythms. The RNA-seq and RT-qPCR data revealed that DEX increases expression of GR-sensitive clock gene Per1 and changes the expression of other genes that may affect the clock (e.g., Hif3a, Klf9, Zbtb16, Mt1-3). The effects were more significant when the treatment timing matched the temporal window of highest sensitivity of the SCN clock to DEX. Our findings advance the largely unexplored field of chrono-ontogenesis and define the effects of DEX on the fetal brain transcriptional landscape, with specific implications for the circadian clock. - Source: PubMed
Publication date: 2026/05/09
Sládek MartinCadenato PedroSemenovykh KaterynaHoudek PavelSumová Alena