TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation of site-specific transgenic mice

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Known as:: TARGATT™ H11 Frozen Embryos (FVB) Academic rapid generation site-specific transgenic mice
Catalog number:: ASC-AST-0002
Product Quantity:: 45 ^ 50 embryos
Category:: -
Supplier:: Gentaur
Gene target:: TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation site-specific transgenic mice

Related genes to: TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation of site-specific transgenic mice

Gene:: MICE ^{NIH gene}
Name:: MHC class I polypeptide-related sequence E (pseudogene)
Previous symbol:: -
Synonyms:: dJ377H14.7, PERB11.5
Chromosome:: 6p22.1
Locus Type:: pseudogene
Date approved:: 1994-09-07
Date modifiied:: 2016-10-05

Related products to: TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation of site-specific transgenic mice

Related articles to: TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation of site-specific transgenic mice

C-176 reduces inflammation-induced pain by blocking the cGAS-STING pathway in microglia.
Inflammatory pain, is caused by lesions or diseases of the somatosensory tissue, is a prevalent chronic condition that profoundly impacts the quality of life. However, clinical treatment for this type of pain remains limited. Traditionally, the stimulation of microglia and subsequent inflammatory reactions are considered crucial elements to promote the worsening of inflammatory pain. Recent research has shown the crucial importance of the cGAS-STING pathway in promoting inflammation. It is still uncertain if the cGAS-STING pathway plays the role in the fundamental cause of inflammatory pain. This research showed that injecting CFA into the left hind paw of mice caused mechanical allodynia and increased inflammation in the spine. Our research results suggested that the cGAS-STING pathway had a function in the inflammation mediated by microglia in the spinal cord dorsal horn. Blocking the cGAS-STING pathway using STING antagonists (C-176) led to reduced release of inflammatory factors and prevented M1 polarization of BV2 microglia in a laboratory setting. Additionally, intrathecal administration of C-176 reduced the allodynia in CFA treated mice. Our results suggest that inhibiting microglial polarization through the cGAS-STING pathway represents a potential novel therapeutic strategy for inflammatory pain. - Source: PubMed
Publication date: 2024/05/13
Yang Shan-MingLi Yuan-BoSi Hua-XingWei YiMa Fu-JuanWang JianChen TaoChen Kun
Treatment of mice with maternal intermittent fasting to improve the fertilization rate and reproduction.
Maternal intermittent fasting (MIF) can have significant effects on several tissue and organ systems of the body, but there is a lack of research on the effects on the reproductive system. So, the aim of our study was to analyze the effects of MIF on fertility. B6C3F1Crl (C57BL/6N × C3H/HeN) male and female mice were selected for the first part of the experiments and were analyzed for body weight and fat weight after administration of the MIF intervention, followed by analysis of sperm counts and activation and embryo numbers. Subsequently, two strains of mice, C57BL/6NCrl and BALB/cJRj, were selected and administered MIF to observe the presence or absence of vaginal plugs for the purposes of mating success, sperm and oocyte quality, pregnancy outcome, fertility status and fertilization (IVF). Our results showed a significant reduction in body weight and fat content in mice receiving MIF intervention in B6C3F1Crl mice. Comparing the reproduction of the two strains of mice. However, the number of litters was increased in all MIF interventions in C57BL/6NCrl, but not statistically significant. In BALB/cJRj, there was a significant increase in the number of pregnant females as well as litter size in the MIF treatment group, as well as vaginal plugs, and IVF. There was also an increase in sperm activation and embryo number and the MIF intervention significantly increased sperm count and activation. Our results suggest that MIF interventions may be beneficial for reproduction in mice. - Source: PubMed
Publication date: 2024/05/13
Wang YananLi XinGong RuitingZhao Yu
Multifactoral immune modulation potentiates durable remission in multiple models of aggressive malignancy.
Tumors typically lack canonical danger signals required to activate adaptive immunity and also frequently employ substantial immunomodulatory mechanisms that downregulate adaptive responses and contribute to escape from immune surveillance. Given the variety of mechanisms involved in shielding tumors from immune recognition, it is not surprising that single-agent immunomodulatory approaches have been largely unsuccessful in generating durable antitumor responses. Here we report a unique combination of immunomodulatory and cytostatic agents that recondition the tumor microenvironment and eliminate complex and/or poor-prognosis tumor types including the non-immunogenic 4T-1 model of TNBC, the aggressive MOC-2 model of HNSCC, and the high-risk MYCN-amplified model of neuroblastoma. A course of therapy optimized for TNBC cured a majority of tumors in both ectopic and orthotopic settings and eliminated metastatic spread in all animals tested at the highest doses. Immune responses were transferable between therapeutic donor and naïve recipient through adoptive transfer, and a sizeable abscopal effect on distant, untreated lesions could be demonstrated experimentally. Similar results were observed in HNSCC and neuroblastoma models, with characteristic remodeling of the tumor microenvironment documented in all model systems. scRNA-seq analysis implicated upregulation of innate immune responses and antigen presentation in tumor cells and the myeloid cell compartment as critical early events. This analysis also highlighted the potential importance of the autonomic nervous system in the governance of inflammatory processes. The data indicate that the targeting of multiple pathways and mechanisms of action can result in substantial synergistic antitumor effects and suggest follow-up in the neoadjuvant setting may be warranted. - Source: PubMed
Halpert Matthew MBurns Briana ARosario Spencer RWithers Henry GTrivedi Akshar JHofferek Colby JGephart Benjamin DWang HaotongVazquez-Perez JonathanAmanya Sharon BHyslop Sean TYang JianhuaKemnade Jan OSandulache Vlad CKonduri VanajaDecker William K
Dietary supplementation with non-digestible isomaltooligosaccharide and ZDY2013 ameliorates DSS-induced colitis modulating intestinal barrier integrity and the gut microbiota.
Non-digestible oligosaccharides have attracted attention due to their critical role in maintaining the balance of a host's gut microbiota. ZDY2013 was isolated from traditional fermented acid beans, which could metabolize many complex carbohydrates and had intestinal immunomodulatory effects. In our study, the ameliorative effect of a combination of non-digestible isomaltooligosaccharide (IMO) and ZDY2013 was investigated in dextran sulfate sodium (DSS)-induced colitis mice. The results showed that IMO could specifically promote ZDY2013 intestinal colonization after five days of gavage and ameliorate the symptoms of colitis (survival rate, DAI score, colon length, .) as well as colon tissue integrity. IMO combined with ZDY2013 increased the levels of intestinal tight junction proteins (ZO-1 and claudin) and mucin (MUC-2), followed by alleviation of inflammatory responses (decreased the expression of IL-1β, TNF-α, and IL-6 and increased the expression of IL-10 and IL-22) and the level of oxidative stress (decreased the level of COX-2 and iNOS and increased the expression of T-AOC and SOD). Furthermore, the combination increased the diversity of the gut microbiota and modulated the microbial structural component (decreased the abundance of and and increased the abundance of and SCFA-producing related species). Taken together, our results suggested that the consumption of IMO and ZDY2013 could improve the symptoms of colitis in mice by improving the intestinal barrier along with regulating the composition and metabolites of the gut microbiota. - Source: PubMed
Publication date: 2024/05/13
Zhang ZhihongHu YingshengZhang NaLi JinmeiLu JinlinWei Hua
Reduced Incretin Receptor Trafficking upon Activation Enhances Glycemic Control and Reverses Obesity in Diet-Induced Obese Mice.
Activation of incretin receptors by their cognate agonists augments sustained cAMP generation both from the plasma membrane as well as from the endosome. To address the functional outcome of this spatiotemporal signaling, we developed a non-acylated glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptor dual agonist I-M-150847 that reduced receptor internalization following activation of the incretin receptors. The incretin receptor dual agonist I-M-150847 was developed by replacing the tryptophan cage of exendin-4 tyrosine substituted at the amino terminus with the C-terminal undecapeptide sequence of oxyntomodulin that placed lysine 30 of I-M-150847 in frame with the corresponding lysine residue of GIP. The peptide I-M-150847 is a partial agonist of GLP-1R and GIPR; however, the receptors, upon activation by I-M-150847, undergo reduced internalization that promotes agonist-mediated iterative cAMP signaling and augments glucose-stimulated insulin exocytosis in pancreatic beta cells. Chronic administration of I-M-150847 improved glycemic control, enhanced insulin sensitivity, and provided profound weight loss in diet-induced obese (DIO) mice. Our results demonstrated that despite being a partial agonist, I-M-150847, by reducing the receptor internalization upon activation, enhanced the incretin effect and reversed obesity. - Source: PubMed
Publication date: 2024/05/13
Bauri RathinBele ShilpakEdelli JhansiReddy Neelesh CKurukuti SreenivasuluDevasia TomIbrahim AhamedRai VishalMitra Prasenjit

TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation of site-specific transgenic mice

Related genes to: TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation of site-specific transgenic mice

Related products to: TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation of site-specific transgenic mice

Related articles to: TARGATT™ H11 Frozen Embryos (FVB) Academic for rapid generation of site-specific transgenic mice

C-176 reduces inflammation-induced pain by blocking the cGAS-STING pathway in microglia.

Treatment of mice with maternal intermittent fasting to improve the fertilization rate and reproduction.

Multifactoral immune modulation potentiates durable remission in multiple models of aggressive malignancy.

Dietary supplementation with non-digestible isomaltooligosaccharide and ZDY2013 ameliorates DSS-induced colitis modulating intestinal barrier integrity and the gut microbiota.

Reduced Incretin Receptor Trafficking upon Activation Enhances Glycemic Control and Reverses Obesity in Diet-Induced Obese Mice.