c_Jun (Phospho_Tyr170) Antibody
- Known as:
- c_Jun (Phospho_Tyr170) Antibody
- Catalog number:
- E011023-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- c_Jun (Phospho_Tyr170) Antibody
Related products to: c_Jun (Phospho_Tyr170) Antibody
Related articles to: c_Jun (Phospho_Tyr170) Antibody
- A search for Higgs boson (H) production in association with two vector bosons (V=W, Z) via vector-boson scattering (VBS) is presented using proton-proton collision data collected at sqrt[s]=13 TeV by the CMS experiment, corresponding to an integrated luminosity of 138 fb^{-1}. Events containing two forward jets consistent with VBS, a large-radius jet from the decay of a boosted H to a pair of b quarks, and zero, one, or two charged leptons coming from V decays are selected. The process is excluded at 95% confidence level for observed (expected) values of the VVHH coupling modifier κ_{2V} outside the interval 0.40<κ_{2V}<1.60 (0.34<κ_{2V}<1.66), assuming standard model values for all other couplings, thus establishing a novel probe of the VVHH interaction. Constraints are also set on the individual κ_{2W} and κ_{2Z} coupling modifiers and on the allowed region in the κ_{2W}-κ_{2Z} plane. - Source: PubMed
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MBloom KClaes D RHaza GHossain JJoo CKravchenko IKwok K H MRohilla ASiado J ETabb WVagnerini AWightman AYan FChiarito BChou J PClark S VDonnelly SGadkari DGershtein YHalkiadakis EHoughton CJaroslawski DKobert ALaflotte ILath AMartins JPerez Prada MRand BReichert JSaha PSalur SSchnetzer SSomalwar SStone RThayil S AThomas SVora JBouchamaoui HDezoort GElmer PFrankenthal AGalli MGreenberg BHaubrich NKennedy KKopp GLai YLange DLoeliger AMarlow DOjalvo IOlsen JSimpson FStickland DTully CBandyopadhyay HHay LHsia H WIashvili IKalogeropoulos AKharchilava AMandal AMorris MNguyen DRappoccio SRejeb Sfar HWilliams AYu DAlexander JChen XDickinson JDuquette AFan JFan XGrassi JHogan SKotamnives PMonroy JNiendorf GOshiro MPatterson J RRyd AThom JWittich PZou RZygala LBessidskaia Bylund OBodek Ade Barbaro PDemina RGarcia-Bellido AHare H SHindrichs OParmar NParygin PSeo HTaus RCarrigan MDe Los Santos RDurkin L SHill CJoyce MWenzl D AWiner B LYates BAlison JAn SCremonesi MDutta VErtorer E YFerguson TGómez Espinosa T AHarilal AKallil Tharayil AKanemura MLiu CMarchegiani MMeiring PMurthy SPalit PPark KPaulini MRoberts ASanchez ATerrill WMalik SSharma RBarone GBenelli GCutts DEllis SGouskos LHadley MHeintz UHo K WKwon TLambrecht LLandsberg GLau K TLuo JMondal SRoloff JRussell TSagir SShen XStamenkovic MVenkatasubramanian NAlly DDelannoy A GFiorendi SHarris JHolmes TKanuganti A RKarunarathna NLawless JLee LNibigira ESkipworth BSpanier SAppelt EChen YGreene SGurrola AJohns WKunnawalkam Elayavalli RMelo ARathjens DRomeo FSheldon PTuo SVelkovska JViinikainen JZhang JAebi DAhmad MAkhter TAndrosov KBasnet ABolshov ABouhali OCagnotta AD'Amante VEusebi RFlanagan PGilmore JGuo YKamon TLuo SMueller RSafonov AAcosta DAgrawal AArbour CCarnahan TDas PEcklund K MGeurts F JHuang TKrommydas ILewis NLi WLin JMiguel Colin OPadley B PRedjimi RRotter JVico Villalba CWulansatiti MYigitbasi EZhang YAkchurin NDamgov JFeng YGogate NJin WKazhykarim YLamichhane KLee S WMadrid CMankel APeltola TVolobouev IAbdullin SBrinkerhoff ACollins EDarwish M RDittmann JHatakeyama KHegde VHiltbrand JMcMaster BSamudio JSawant SSutantawibul CWilson JCardwell BChung HCox BHakala JHamilton Ilha Machado GHirosky RJose MLedovskoy AMantilla CNeu CRamón Álvarez CWu ZAravind ABanerjee SBlack KBose TChavez EDasu SEveraerts PGalloni CHe HHerndon MHerve AKoraka C KLomte SLoveless RMallampalli AMohammadi AMondal SNelson TParida GPinna DPétré LSavin AShang VSharma VSmith W HTeague DTsoi H FVetens WWarden ADudko LKim VMurzin VOreshkin VSosnov DAfanasiev SAlexakhin VAndreev YAushev TBudkouski DChistov RDanilov MDimova TErshov AGninenko SGorbunov IGribushin AKamenev AKarjavine VKirsanov MKlyukhin VKodolova OKorenkov VKorsakov IKozyrev AKrasnikov NLanev AMalakhov AMatveev VNikitenko APalichik VPerelygin VPetrushanko SRadchenko OSavina MShalaev VShmatov SShulha SSkovpen YSlizhevskiy KSmirnov VTeryaev OTlisova IToropin AVoytishin NZarubin AZhizhin IBoos EBunichev VDubinin MSavrin VSnigirev A - Huwang Mingmu decoction (HWMMT) is a traditional Chinese herbal formula used clinically for diabetic retinopathy (DR), but its neuroprotective mechanisms remain unclear. This study aimed to investigate whether HWMMT protects retinal neurons in early DR by attenuating glutamate excitotoxicity via the IL-1β/c-Jun/glutamine synthetase (GS) signaling axis. Diabetes was induced in Sprague-Dawley rats by streptozotocin injection, and animals were randomized into control, diabetic model (DM), and HWMMT-treated diabetic (DM + HWMMT) groups. HWMMT was orally administered for 8 wk, with body weight and blood glucose monitored weekly. At weeks 4 and 8, retinal tissues and serum were collected for qRT-PCR, Western blotting, and ELISA. In vitro, primary rat retinal Müller glial cells (Müller) were cultured and assigned to five groups: blank control, HWMMT serum control, high-glucose (HG), HG + HWMMT, and HG + HWMMT + IL-1β (rescue group). Cell viability, LDH release, glutamate secretion, apoptosis, and expression of IL-1β, c-Jun, and GS were evaluated. In vivo, DM rats showed slower weight gain, sustained hyperglycemia, upregulated retinal IL-1β and c-Jun expression, downregulated GS, and elevated serum glutamate; HWMMT treatment significantly reversed these abnormalities. In vitro, HG exposure decreased Müller cell viability, increased apoptosis, LDH leakage and glutamate release, and induced IL-1β/c-Jun upregulation with GS downregulation; co-treatment with HWMMT-containing serum reversed all these changes. Notably, exogenous IL-1β supplementation significantly attenuated the cytoprotective and anti‑apoptotic effects of HWMMT and reversed its modulation of IL-1β, c-Jun, GS, and glutamate homeostasis. Collectively, these findings demonstrate that HWMMT exerts neuroprotection in early DR by suppressing the IL-1β/c-Jun signaling cascade and restoring GS expression and function in Müller cells, thereby reducing extracellular glutamate accumulation and mitigating excitotoxic damage. The rescue experiments further support that HWMMT acts specifically through this pathway, providing mechanistic insight and preclinical evidence for HWMMT as a potential therapeutic intervention for early diabetic retinopathy. - Source: PubMed
Publication date: 2026/09/18
Qin XueweiWang LiminYao XianfengChen MeiZheng KaijinZheng Li - Meckel's diverticulum (MD) is the most common congenital gastrointestinal malformation. Balloon-assisted enteroscopy (BAE) permits direct visualization in adults, but no standardized endoscopic classification exists. We developed an endoscopic framework for adult MD and evaluated its clinical utility and association with disease severity. - Source: PubMed
Publication date: 2026/09/18
Yang JingYin XinZhao Hai-YanFan YanZhou LeiXu DanWei Wan-HuiYan Jun-WeiFan Chao-QiangNing Shou-BinZhang Heng - Alcohol contributes to the progression of steatotic liver disease. However, in individuals with MetALD, the impact of changes in drinking behavior on disease progression remains unclear. We investigated whether longitudinal changes in alcohol consumption were associated with the risk of major adverse liver outcomes (MALO) in people with MetALD. - Source: PubMed
Publication date: 2026/09/18
Lee Jun-HyukPark JiminAhn Sung HoJeon So YoungLee Hye SunLee JonghyunKim JonghyunLee Hyo YoungYoon Eileen LJun Dae Won - Membrane associated guanylate kinase WW and PDZ domain containing 3 (MAGI3) functions as a tumor suppressor in lung cancer, but its role and mechanism in non‑small cell lung cancer (NSCLC) progression remain unclear. MAGI3 expression was detected in NSCLC tissues (immunohistochemistry) and cell lines (western blotting). Tet‑on inducible MAGI3 overexpression was used to assess effects on NSCLC cells via Cell Counting Kit‑8, Transwell, colony/sphere formation, β‑Galactosidase staining and flow cytometry. Ubiquitination/half‑life assays analyzed MAGI3‑TAZ (transcriptional co‑activator with PDZ‑binding motif) interaction. and xenograft tumor models evaluated tumor growth and metastasis. The Cancer Genome Atlas data, clinical samples, and cell lines showed downregulated MAGI3 in NSCLC, correlating with poor prognosis. MAGI3 overexpression reduced cell viability, clonogenicity, sphere formation, migration and invasion; induced G1 phase arrest (reduced CyclinD1) and cellular senescence. MAGI3 specifically promoted TAZ ubiquitination via PDZ domain‑mediated interaction, which subsequently blocked β‑catenin nuclear translocation, dampened Wnt signaling components (DVL2/phosphorylated GSK3β), and reduced TCF/LEF transcriptional output. Reconstitution of TAZ reversed MAGI3‑mediated inhibition of Wnt pathway markers (cMYC, c‑JUN, WISP1 and PPARD). , MAGI3 overexpression suppressed tumor growth and lung metastasis, while MAGI3 silencing increased metastatic nodules. The present study identified that MAGI3, as a suppressor in NSCLC progression, repressed the Wnt pathway‑including TAZ degradation, impaired β‑catenin nuclear translocation, and diminished TCF/LEF transcription‑thereby restraining tumorigenesis and metastasis of NSCLC. - Source: PubMed
Publication date: 2026/09/18
Liang YeZhuang Jie