Mouse Target of EGR1 protein 1(TOE1) ELISA kit SpeciesMouse
- Known as:
- Mouse Target EGR1 protein 1(TOE1) Enzyme-linked immunosorbent assay test reagent SpeciesMouse
- Catalog number:
- CSB-EL024041MO
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- Cusabio
- Gene target:
- Mouse Target EGR1 protein 1(TOE1) ELISA kit SpeciesMouse
Related genes to: Mouse Target of EGR1 protein 1(TOE1) ELISA kit SpeciesMouse
- Gene:
- EGR1 NIH gene
- Name:
- early growth response 1
- Previous symbol:
- -
- Synonyms:
- TIS8, G0S30, NGFI-A, KROX-24, ZIF-268, AT225, ZNF225
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-11
- Date modifiied:
- 2016-10-05
Related products to: Mouse Target of EGR1 protein 1(TOE1) ELISA kit SpeciesMouse
Related articles to: Mouse Target of EGR1 protein 1(TOE1) ELISA kit SpeciesMouse
- Depression is a devastating mood disorder that causes significant disability worldwide. Current knowledge of its pathophysiology remains modest and clear biological markers are lacking. Emerging evidence from human and animal models reveals persistent alterations in endoplasmic reticulum (ER) homeostasis, suggesting that ER stress-related signaling pathways may be targets for prevention and treatment. However, the neurobiological basis linking the pathways involved in depression-related ER stress remains unknown. Here, we report that an induced model of ER stress in mouse serotonin (5-HT) neurons is associated with reduced Egr1-dependent 5-HT cellular activity and 5-HT neurotransmission, resulting in neuroplasticity deficits in forebrain regions and a depressive-like phenotype. Ketamine administration engages downstream eIF2α signaling to trigger rapid neuroplasticity events that rescue the depressive-like effects. Collectively, these data identify ER stress in 5-HT neurons as a cellular pathway involved in the pathophysiology of depression and show that eIF2α is critical in eliciting ketamine's fast antidepressant effects. - Source: PubMed
Publication date: 2024/04/18
Miquel-Rio LluisSarriés-Serrano UnaiSancho-Alonso MaríaFlorensa-Zanuy EvaPaz VerónicaRuiz-Bronchal EstherManashirov SharonCampa LeticiaPilar-Cuéllar FuencislaBortolozzi Analia - Immediate early genes (IEGs) are rapidly activated and initiate diverse cellular processes including neuroplasticity. We report the effect of psilocybin (PSIL), PSIL-containing psychedelic mushroom extract (PME) and 5-hydroxytryptophan (5-HTP) on expression of the IEGs, , and in mouse somatosensory cortex (SSC). In our initial experiment, male C57Bl/6j mice were injected with PSIL 4.4 mg/kg or 5-HTP 200 mg/kg, alone or immediately preceded by serotonergic receptor modulators. IEG mRNA expression 1 hour later was determined by real time qPCR. In a replication study a group of mice treated with PME was added. In our initial experiment, PSIL but not 5-HTP significantly increased expression of all three IEGs. No correlation was observed between the head twitch response (HTR) induced by PSIL and its effect on the IEGs. The serotonergic receptor modulators did not significantly alter PSIL-induced IEG expression, with the exception of the 5-HT2C antagonist (RS102221), which significantly enhanced PSIL-induced egr2 expression. 5-HTP did not affect IEG expression. In our replication experiment, PSIL and PME upregulated levels of and while the upregulation of was not significant. We have shown that PSIL and PME but not 5-HTP (at a dose sufficient to induce HTR), induced a significant increase in and expression in mouse SSC. Our findings suggest that and expression may be associated with psychedelic effects. - Source: PubMed
Publication date: 2024/04/18
Lerer EladBotvinnik AlexanderShahar OrrGrad MeitarBlakolmer KarinShomron NoamLotan AmitLerer BernardLifschytz Tzuri - Atherosclerosis, the main underlying pathology of cardiovascular disease, is a chronic inflammatory disease characterized by lipid accumulation and immune cell responses in the vascular wall, resulting in plaque formation. It is well-known that atherosclerosis prevalence and manifestation vary by sex. However, sexual dimorphism in the immune landscape of atherosclerotic plaques has up to date not been studied at high-resolution. In this study, we investigated sex-specific differences in atherosclerosis development and the immunological landscape of aortas at single-cell level in aged Ldlr mice. - Source: PubMed
Publication date: 2024/05/02
Smit Virginiade Mol JillKleijn Mireia N A BernabéDepuydt Marie A Cde Winther Menno P JBot IlzeKuiper JohanFoks Amanda C - Cancer-associated fibroblasts (CAFs) exhibit notable versatility, plasticity, and robustness, actively participating in cancer progression through intricate interactions within the tumor microenvironment (TME). N6-methyladenosine (mA) modification is the most prevalent modification in eukaryotic mRNA, playing essential roles in mRNA metabolism and various biological processes. Howbeit, the precise involvement of mA in CAF activation remains enigmatic. In this study, we revealed that the mA demethylase FTO supports CAF-mediated angiogenesis through activation of EGR1 and VEGFA in conjunctival melanoma (CoM). First, single-cell transcriptome analysis revealed that FTO was specifically upregulated in the CAF population, thereby contributing to the hypo-mA status in the TME of CoM. Moreover, CAFs of CoM displayed extensive proangiogenic potential, which was largely compromised by FTO inhibition, both in vitro and in vivo. By employing multi-omics analysis, we showed that FTO effectively eliminates the mA modifications of VEGFA and EGR1. This process subsequently disrupts the YTHDF2-dependent mRNA decay pathway, resulting in increased mRNA stability and upregulated expression of these molecules. Collectively, our findings initially indicate that the upregulation of FTO plays a pivotal role in tumor development by promoting CAF-mediated angiogenesis. Therapeutically, targeting FTO may show promise as a potential antiangiogenic strategy to optimize cancer treatment. - Source: PubMed
Publication date: 2024/04/27
Liao QiliShi HanhanYang JieGe ShengfangJia RuobingSong XinChai PeiweiJia Renbing - Shear stress during bioreactor cultivation has significant impact on cell health, growth, and fate. Mammalian cells, such as T cells and stem cells, in next-generation cell therapies are especially more sensitive to shear stress present in their culture environment than bacteria. Therefore, a base knowledge about the shear stress imposed by the bioprocesses is needed to optimize the process parameters and enhance cell growth and yield. However, typical computational flow dynamics modeling or PCR-based assays have several limitations. Implementing and interpreting computational modeling often requires technical specialties and also relies on many simplifications in modeling. PCR-based assays evaluating changes in gene expression involve cumbersome sample preparation with the use of advanced lab equipment and technicians, hampering rapid and straightforward assessment of shear stress. Here, we developed a simple, cell-based shear stress sensor for measuring shear stress levels in different bioreactor types and operating conditions. We engineered a CHO-DG44 cell line to make its stress sensitive promoter EGR-1 control GFP expression. Subsequently, the stressed CHO cells were transferred into a 96 well plate, and their GFP levels (population mean fluorescence) were monitored using a cell analysis instrument (Incucyte®, Sartorius Stedim Biotech) over 24hours. After conducting sensor characterization, which included chemical induced stress and fluid shear stress, and stability investigation, we tested the shear stress sensor in the Ambr® 250 bioreactor vessels (Sartorius Stedim Biotech) with different impeller and vessel designs. The results showed that the CHO cell-based shear stress sensors expressed higher GFP levels in response to higher shear stress magnitude or exposure time. These sensors are useful tools to assess shear stress imposed by bioreactor conditions and can facilitate the design of various bioreactor vessels with a low shear stress profile. - Source: PubMed
Publication date: 2024/04/27
Kwon TaehongLeroux Ann-CathrinZang HanPollard DavidZehe ChristophAkbari Samin