IL-7, His, Mouse Protein
- Known as:
- Interleukin-7, histidine, Mouse Protein
- Catalog number:
- z03209-50
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- IL-7 His Mouse Protein
Related genes to: IL-7, His, Mouse Protein
- Gene:
- IL7 NIH gene
- Name:
- interleukin 7
- Previous symbol:
- -
- Synonyms:
- IL-7
- Chromosome:
- 8q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-10-12
- Date modifiied:
- 2016-10-11
- Gene:
- IL7R NIH gene
- Name:
- interleukin 7 receptor
- Previous symbol:
- -
- Synonyms:
- CD127, IL7RA
- Chromosome:
- 5p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2019-04-23
Related products to: IL-7, His, Mouse Protein
Related articles to: IL-7, His, Mouse Protein
- Antipsychotic-induced weight gain (AIWG) is a major clinical concern in schizophrenia spectrum disorders. While inflammatory pathways are implicated, it is unclear whether baseline variation in these processes contributes to individual susceptibility to early weight gain. An antipsychotic quasi-naïve sample of first-episode patients treated with the same antipsychotic is ideal to evaluate this association. - Source: PubMed
Publication date: 2026/08/28
Dielemans Daphne A MHuizer Karinvan der Pluijm MariekeThijssen Andreavan Beveren Nico J Mde Haan Lieuwe - Breast cancer is among the leading causes of cancer mortality worldwide, with aging as a major risk factor. Caloric restriction (CR) is a well-established non-pharmaceutical intervention that extends healthspan and delays tumorigenesis, yet the systemic molecular mechanisms remain elusive. Both chronic and intermittent CR influence metabolic homeostasis, but their long-term effects on circulating miRNAs in breast cancer predisposition are unclear. Here, we examined how chronic and intermittent CR and subsequent refeeding remodel circulating miRNA networks in a tumor-free, female breast cancer-prone transgenic mouse model. Blood samples were collected and circulating miRNA expression levels were determined at weeks 10 (young), 49 (adult), and 81 (old) using GeneChip miRNA 4.1 Array. Differential expression and target enrichment analysis were performed to identify age- and diet-associated modulatory patterns. Aging significantly altered the global circulating miRNA profile and validated targets were enriched in the IL-7 signaling, GPCR signaling, and TCA cycle. Both chronic and intermittent CR reshaped these age-associated alterations, with the consistent target pathways. The effects were most pronounced at adult age rather than old age, while the refeeding phase of the intermittent CR partially preserved the CR-induced miRNA patterns. Integrative analyses identified three key miRNAs (mmu-miR-142-5p, mmu-miR-30e-5p, mmu-miR-494-3p), where CR reversed the expression patterns induced by aging, suggesting a shared molecular mechanism. Our findings demonstrate that chronic and intermittent CR modulate circulating miRNAs in an age-dependent manner in female transgenic breast cancer-prone mice. - Source: PubMed
Publication date: 2026/08/27
Tuna Bilge GuvencKeles Nazim ArdaCicekdal Munevver BurcuOzorhan UmitThomas Pınar BuketKuskucu AysegulBayrak Omer FarukYilmaz BayramDogan Soner - Ischemia/Reperfusion (I/R) and the increasing age of patients are coexisting challenges in today's cardiovascular medicine. Vascular I/R leads to endothelial dysfunction and is partially driven by inflammation. With increasing age, a profile of biomolecules known as the senescence-associated secretory phenotype (SASP) also increases. The SASP correlates with decreased resilience and intrinsic capacity to withstand various stressors and contains pro-inflammatory cytokines, likely fueling I/R injury. Senomorphics block SASP secretion. We investigated the effect of ruxolitinib on endothelial function after vascular I/R injury in middle-aged and old mice. - Source: PubMed
Publication date: 2026/08/22
Saemann LarsSoyer Hatice SedaPohl SabineHagewiesche SaskiaSarow LeahWambrauw SaraKuru-Schors MerveSimm Andreas - Yeast-derived postbiotic dietary supplements are increasingly recognized as bioactive nutritional components capable of modulating immune function through host-microbial interactions. - Source: PubMed
Publication date: 2026/08/06
Jensen Gitte SCruickshank David DGrinage Earvin A FCruickshank DinaSanchez KristaGarcia-Campayo VicentaPaton Neil DGreen Justin B - Persistent inflammation, immunosuppression, and catabolism syndrome (PIICS) is a major cause of prolonged morbidity and poor outcomes among critical illness survivors. We established long-term murine PIICS models using two peritonitis-induced sepsis methods-cecal ligation and puncture (CLP) and fecal suspension intraperitoneal injection (FSI)-and investigated their immunological and histopathological features over 2 months. Survivors were defined as PIICS model mice, with unoperated mice serving as controls. Following an intraperitoneal lipopolysaccharide (LPS; 10 mg/kg) challenge, 27 plasma cytokines and chemokines were quantified before and 20 h after administration, and survival was monitored for 14 days. Survivors of CLP and FSI exhibited sustained baseline elevations in inflammatory mediators (G-CSF, IL-7, CCL3/4) and reductions in anti-inflammatory cytokines (IL-13, TGF-β2) compared with those in controls. Following the LPS challenge, control mice showed robust cytokine induction, and 4 of 13 died, whereas both PIICS groups exhibited globally suppressed cytokine responses with no mortality (p = 0.011 vs. controls). Histopathological staining showed mild splenic macrophage infiltration at baseline in both PIICS groups. Upon LPS administration, pulmonary congestion, splenic macrophage infiltration, and neutrophil infiltration into the portal vein were observed. Intra-abdominal abscesses or granuloma-like masses occurred in 50% of CLP-PIICS mice. Collectively, these long-term PIICS models recapitulate key clinical features, including persistent dysregulated inflammation, impaired responsiveness to secondary stimuli, and chronic tissue pathology, providing a platform to investigate the transition from acute sepsis to PIICS and for preclinical testing of immune-restorative or metabolic interventions in survivors of sepsis. - Source: PubMed
Publication date: 2026/08/20
Tsuchida TakumiWada TakeshiMizugaki AsumiOda YoshitakaKayano KatsuhideYamakawa KazumaTanaka Shinya