Anti_Mouse, mab IL_3R Source Rat
- Known as:
- Anti_Mouse, mab IL_3R Source Rat
- Catalog number:
- 103-M421
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab IL_3R Source Rat
Related genes to: Anti_Mouse, mab IL_3R Source Rat
- Gene:
- CSF2RB NIH gene
- Name:
- colony stimulating factor 2 receptor beta common subunit
- Previous symbol:
- IL3RB
- Synonyms:
- IL5RB, CD131, betaGMR
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2017-07-12
Related products to: Anti_Mouse, mab IL_3R Source Rat
Related articles to: Anti_Mouse, mab IL_3R Source Rat
- Warm diseases in swine, particularly those associated with highly pathogenic viruses such as African swine fever virus (ASFV) and porcine reproductive and respiratory syndrome virus (PRRSV), inflict devastating economic losses on global pork production. Current control strategies rely heavily on antibiotics and vaccines; however, emerging antimicrobial resistance and vaccine efficacy variability necessitate alternative therapeutic approaches. Traditional Chinese Veterinary Medicine offers potential solutions, yet rigorous evidence-based studies are required to meet modern regulatory standards. This study aimed to investigate Qingying granules, a novel veterinary formulation derived from the classic Qingying decoction, for the treatment of warm disease in pigs and to elucidate its molecular mechanisms through multi-omics analysis. - Source: PubMed
Publication date: 2026/06/30
Yan ZunxiangLin ShuqianQiao HongzhiZhao ZengchengYin BinYang ShifaLi KaiyuanLiu Yueyue - Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Acute respiratory failure frequently occurs due to leukemia infiltration of the lungs. Underlying mechanisms remain unexplored and therapeutic interventions remain empiric. Here we map the AML lung microenvironment at spatial and single-cell resolution. We show that extensive remodeling is coupled with inflammation and impaired tissue integrity and function. Steroid treatment significantly reduces AML burden and lung infiltration, improving oxygenation and pulmonary function. As a mechanistic correlate, the S-type lectin Lgals9 is triggered by inflammation and mediates cell-cell interactions within infiltrated lungs. Also, the alarmin IL-33 and its receptor (IL-1RL1) are involved in cell-cell interactions within the leukemic lung microenvironment. Targeting either the Lgals9 or IL-33 axis significantly decreases overall AML burden and lung infiltration through effects on both the immune microenvironment and AML cells. Our studies delineate pulmonary infiltration phenotypes in acute leukemia, enabling new treatment strategies. - Source: PubMed
Publication date: 2026/06/29
Paraskevopoulou VarvaraLin ZiyanCasado-Pelaez MartaGrases DanielaAl-Santli WafaBalandrán Juan CarlosZhou FangRashidfarrokhi AliCross MichaelYeung Stephen TNtatsoulis KonstantinosPatel TejasChen XufengNicolet DeedraEscobosa MarcPorta EduardTrowbridge Jennifer JKhanna Kamal MPapagiannakopoulos ThalesMoreira Andre LKanagal-Shamanna RashmiLoghavi SanamTsirigos ArisEisfeld Ann-KathrinEsteller ManelAifantis Iannis - A better understanding of the response of granulosa cells to exogenous hormone stimulation and how this impacts the complex interplay between the granulosa cells and the oocyte is crucial for the optimal management of infertile couples seeking IVF treatment. - Source: PubMed
Publication date: 2026/06/10
Medica AlexaKim Matthew EHung Wei-TingSohni AbhishekDuleba AntoniTan KunWilkinson Miles F - Osteoporosis is a metabolic bone disorder characterized by reduced bone mass and deterioration of bone microarchitecture, resulting in increased skeletal fragility and an elevated risk of fracture. Its initiation and progression are closely linked to immune dysregulation and chronic inflammation. Interleukin-33 (IL-33), a key member of the interleukin-1 cytokine family, was initially identified as an alarmin that promotes type 2 immune responses. However, accumulating evidence has demonstrated that IL-33 plays a complex and pivotal role in the regulation of bone homeostasis, making it a molecule of considerable interest in osteoimmunology. This review aims to systematically summarize the mechanisms by which the IL-33/ST2 signaling axis regulates bone metabolism, further elucidate its multifaceted roles in primary and secondary osteoporosis, analyze its dual effects on bone protection and bone destruction, and evaluate its potential, as well as the associated challenges, as a diagnostic biomarker and therapeutic target. - Source: PubMed
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Zhou LiboLiu ZhongchengLiu ZiruiWen LeiGeng BinXia Yayi - Although transplantation is the preferred treatment for end-stage organ disease, long-term outcomes are limited by immunosuppressive drug toxicity and immune-mediated injury. Selective in vivo expansion of regulatory T cells (Tregs) using interleukin-2 (IL-2) analogs has emerged as a strategy to induce antigen-specific transplant tolerance with fewer side effects. Herein, we investigate the therapeutic efficacy of an IL-2 mutein molecule (mIL-2) with enhanced receptor specificity and extended half-life in murine models of solid organ transplantation. mIL-2 therapy significantly improves allograft survival in an antigen-specific manner, accompanied by increased Treg activation, decreased effector T cell activation and reduced donor-specific antibody production. Transcriptional profiling reveals expansion of Tregs expressing the suppression of tumorigenicity 2 (ST2) Tregs with heightened activation status and suppressive function. Accordingly, the mIL-2-induced long-term allograft survival is abrogated in Treg-specific ST2 knockout graft recipients, underscoring the critical role of ST2 Tregs. These findings identify mIL-2 as an approach to promote long-term transplant tolerance while reducing reliance on conventional immunosuppression. - Source: PubMed
Publication date: 2026/06/22
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