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The role of PDIA3 in myogenesis during muscle regeneration.

Beta 3 (β3) integrin plays an important role in the initiation of myogenesis in adult muscle. Protein disulfide isomerases (PDIs) can activate β3 integrin in various cells to promote cell migration, adhesion and fusion. However, the effect of PDIs on myogenesis during muscle regeneration has not been elucidated. Here, we report that PDIA3 expression is induced in regenerating myofibers. The inhibition of PDIA3 in muscle injuries in mice disrupts myoblast differentiation, impairs muscle regeneration, and ultimately aggravates muscle damage. Moreover, PDIA3 expression is upregulated and observed on the cell surfaces of myoblasts during differentiation and fusion. The inhibition of extracellular PDIA3 with an anti-PDIA3 monoclonal antibody attenuates β3 integrin/AKT/mTOR signal activity, inhibits myoblast differentiation, and blocks the fusion of myoblasts. Thus, PDIA3 may be a mediator of myoblast differentiation and fusion during muscle regeneration.

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FDA Standard Frozen Tissu Thermal Shaker with cooli Anti beta3 AR Human, Poly FDA Standard Frozen Tissu FDA Standard Frozen Tissu Zearalenone Mycotoxins EL FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu T-2 Toxin Mycotoxins ELIS MultiGene Gradient therm Multiple organ tumor tiss

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Anti-GPC3 single-chain scFv antibody acts as an agent for radio-immunoimaging in diagnosing hepatocellular carcinoma.

Glypican-3 (GPC3) over-expresses in hepatocellular carcinoma (HCC), but not expresses or under-expresses in normal adult hepatocytes. Therefore, GPC3 acts as a potential target for diagnosis and treatment of HCC. This study aimed to conduct radio-immunoimaging using GPC3 as a target in order, and to explore its potential for diagnosing and treating HCC. Humanized single-chain antibody scFv for HCC was established using phage antibody library. HB2151 was infected with recombinant phage antibodies that are considered to be strongly positive by phage ELISA. Then, the soluble antibodies were obtained post IPTG induction. Soluble antibodies were detected using SDS-PAGE assay. Anti-GPC3 single-chain antibodies were labeled using I, and then the distribution of radioactive markers in nude mice were analyzed by radio-immunoimaging. The results indicated that the size of soluble scFv products was 30 kD after purifying anti-GPC3 scFv antibodies that are successfully screened from phage antibody library. Anti-GPC3 phage antibodies could specifically bind to HCC cells. The ratios of radioactive tumor/blood and tumor/muscle for I labeled anti-GPC3 monoclonal antibodies were increased gradually, achieving the highest at 48 h. Radio-immunoimaging showed that the radioactive uptake of tumor sites remained the strongest at 48 h, and the ratio of target to non-target was the highest. In conclusion, the established anti-GPC3 scFv antibody had the potential to become an agent for radio-immunoimaging in diagnosing HCC and act as a targeted antibody for further radio-immunotherapy of HCC.

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Hepatocellular carcinoma Hepatocellular carcinoma Rabbit Anti-G protein alp Rabbit Anti-Phospho-INPPL Rabbit Anti-glypican 3 GP Rabbit Anti-Cell death in Mouse anti-mouse type II Rabbit Anti-D.Aspartic ac Colon carcinoma tissue ar Mouse anti-chick type I c Rabbit Anti-Insulin Recep Rabbit Anti-intestinal FA

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Production of TRPV2-targeting functional antibody ameliorating dilated cardiomyopathy and muscular dystrophy in animal models.

Abnormal Ca handling is essential in the pathophysiology of degenerative muscle disorders, such as dilated cardiomyopathy (DCM) and muscular dystrophy (MD). Transient receptor potential cation channel, subfamily V, member 2 (TRPV2) is a candidate for Ca entry and a potential therapeutic target for degenerative muscle disorders, there are few specific inhibitors for TRPV2. In this study, we produced a monoclonal antibody (designated mAb88-2) and two polyclonal antibodies (pAb591 and pAb592) that selectively recognize TRPV2 from the outside of cells and interact with the turret region of the pore-forming outer gate. These antibodies inhibited Ca influx via TRPV2 in cultured cells and substantially reduced TRPV2 in the plasma membrane via cellular internalization. We evaluated the therapeutic efficacy of the functional antibody in δ-sarcoglycan-deficient hamster (J2N-k) models of DCM and MD and in the 4C30 DCM model of murine heart failure. The intraperitoneal administration of the functional antibody (0.5 mg/kg) for 2 weeks (once a week) prevented the progression of cardiac dysfunction, as evaluated by echocardiography and histological staining, and improved the abnormal Ca handling (high diastolic Ca level and small Ca transient peak) in cardiomyocytes isolated from J2N-k hamsters and prevented skeletal muscle damage. Further, the antibody effectively prevented heart failure in the 4C30 mouse model with end-stage DCM. Interestingly, endogenous TRPV2 that accumulated in the cardiac and skeletal muscle sarcolemma disappeared upon antibody administration. Thus, the newly produced antibodies are capable of ameliorating DCM and MD by promoting the cellular internalization of TRPV2; antibodies specific to human TRPV2 may substantially improve the treatment of patients with degenerative muscle diseases.

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CDKN1A & CCNA1 Protein Pr Rabbit Anti-Integrin β2 JUP & APC Protein Protein MMP2 & TGFB1 Protein Prot FAS & CTNNB1 Protein Prot Rabbit Anti-Insulin Polyc TP53 & LAMA4 Protein Prot Rabbit Anti-APIP Apaf1 In FGFR2 & FGF10 Protein Pro AKT1 & FRAP1 Protein Prot Rabbit Anti-Integrin beta alkaline phosphatase (int

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LNA-anti-miR-150 ameliorated kidney injury of lupus nephritis by inhibiting renal fibrosis and macrophage infiltration.

The prevalence of lupus nephritis (LN) remains high despite various emerging monoclonal antibodies against with targeting systemic lupus erythematosus (SLE). Renal fibrosis is the main feature of late stage LN, and novel therapeutic agents are still needed. We previously reported that microRNA (miR)-150 increases in renal biopsies of American LN patients and that miR-150 agonist promotes fibrosis in cultured kidney cells. Presently, we aim to verify whether locked nucleic acid (LNA)-anti-miR-150 can ameliorate LN in mice and to investigate its corresponding mechanisms.

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Multifaceted antibodies development against synthetic α-dystroglycan mucin glycopeptide as promising tools for dystroglycanopathies diagnostic.

Dystroglycanopathies are diseases characterized by progressive muscular degeneration and impairment of patient's quality of life. They are associated with altered glycosylation of the dystrophin-glycoprotein (DGC) complex components, such as α-dystroglycan (α-DG), fundamental in the structural and functional stability of the muscle fiber. The diagnosis of dystroglycanopathies is currently based on the observation of clinical manifestations, muscle biopsies and enzymatic measures, and the available monoclonal antibodies are not specific for the dystrophic hypoglycosylated muscle condition. Thus, modified α-DG mucins have been considered potential targets for the development of new diagnostic strategies toward these diseases. In this context, this work describes the synthesis of the hypoglycosylated α-DG mimetic glycopeptide NHAc-Gly-Pro-Thr-Val-Thr[αMan]-Ile-Arg-Gly-BSA (1) as a potential tool for the development of novel antibodies applicable to dystroglycanopathies diagnosis. Glycopeptide 1 was used for the development of polyclonal antibodies and recombinant monoclonal antibodies by Phage Display technology. Accordingly, polyclonal antibodies were reactive to glycopeptide 1, which enables the application of anti-glycopeptide 1 antibodies in immune reactive assays targeting hypoglycosylated α-DG. Regarding monoclonal antibodies, for the first time variable heavy (VH) and variable light (VL) immunoglobulin domains were selected by Phage Display, identified by NGS and described by in silico analysis. The best-characterized VH and VL domains were cloned, expressed in E. coli Shuffle T7 cells, and used to construct a single chain fragment variable that recognized the Glycopeptide 1 (GpαDG1 scFv). Molecular modelling of glycopeptide 1 and GpαDG1 scFv suggested that their interaction occurs through hydrogen bonds and hydrophobic contacts involving amino acids from scFv (I51, Y33, S229, Y235, and P233) and R8 and α-mannose from Glycopeptide 1.

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Custom Immunoassay Develo Peptoid Ligand Assay Deve Goat Anti-Human, Mouse, R Goat Anti-Human AS160 TBC anti-5Methylcytosine anti Goat Anti- Cyt19 AS3MT, ( Glucose Assay With the La Rat monoclonal anti mouse Astrovirus antibody, Mono Cultrex In Vitro Angiogen Goat Anti-Human ASF1A HSP Rabbit Anti-Human ASK1 (p

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Antibody-induced crosslinking and cholesterol-sensitive, anomalous diffusion of nicotinic acetylcholine receptors.

Synaptic strength depends on the number of cell-surface neurotransmitter receptors in dynamic equilibrium with intracellular pools. Dysregulation of this homeostatic balance occurs, for example in myasthenia gravis, an autoimmune disease characterized by a decrease in the number of postsynaptic nicotinic acetylcholine receptors (nAChRs). Monoclonal antibody mAb35 mimics this effect. Here we use STORM nanoscopy to characterize the individual and ensemble dynamics of monoclonal antibody-crosslinked receptors in the clonal cell line CHO-K1/A5, which robustly expresses adult muscle-type nAChRs. Antibody labeling of live cells results in 80% receptor immobilization. The remaining mobile fraction exhibits a heterogeneous combination of Brownian and anomalous diffusion. Single-molecule trajectories exhibit a two-state switching behavior between free Brownian walks and anticorrelated walks within confinement areas. The latter act as permeable fences (~34 nm radius, ~400 ms lifetime). Dynamic clustering, trapping, and immobilization also occur in larger nanocluster zones (120-180 nm radius) with longer lifetimes (11 ± 1 s), in a strongly cholesterol-sensitive manner. Cholesterol depletion increases the size of the clustering phenomenon; cholesterol enrichment has the opposite effect. The disclosed high proportion of monoclonal antibody-crosslinked immobile receptors, together with their anomalous, cholesterol-sensitive diffusion and clustering, provides new insights into the antibody-enhanced antigenic modulation that leads to physiopathological internalization and degradation of receptors in myasthenia.

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Leptin ELISA Kit, Human A Anti AGO2 Mouse, Monoclon Anti-AICDA(Activation-ind Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Androgen Receptor (Phosph Acetylcholine Receptor B Androgen Receptor (Ab-650 Acetylcholinesterase(ACHE Primary antibody DR3 Ant Androgen Receptor , Mouse Androgen Receptor (Phosph

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Clinical efficacy and biomarker analysis of neoadjuvant atezolizumab in operable urothelial carcinoma in the ABACUS trial.

Antibodies targeting PD-1 or its ligand 1 PD-L1 such as atezolizumab, have great efficacy in a proportion of metastatic urothelial cancers. Biomarkers may facilitate identification of these responding tumors. Neoadjuvant use of these agents is associated with pathological complete response in a spectrum of tumors, including urothelial cancer. Sequential tissue sampling from these studies allowed for detailed on-treatment biomarker analysis. Here, we present a single-arm phase 2 study, investigating two cycles of atezolizumab before cystectomy in 95 patients with muscle-invasive urothelial cancer (ClinicalTrials.gov identifier: NCT02662309). Pathological complete response was the primary endpoint. Secondary endpoints focused on safety, relapse-free survival and biomarker analysis. The pathological complete response rate was 31% (95% confidence interval: 21-41%), achieving the primary efficacy endpoint. Baseline biomarkers showed that the presence of preexisting activated T cells was more prominent than expected and correlated with outcome. Other established biomarkers, such as tumor mutational burden, did not predict outcome, differentiating this from the metastatic setting. Dynamic changes to gene expression signatures and protein biomarkers occurred with therapy, whereas changes in DNA alterations with treatment were uncommon. Responding tumors showed predominant expression of genes related to tissue repair after treatment, making tumor biomarker interpretation challenging in this group. Stromal factors such as transforming growth factor-β and fibroblast activation protein were linked to resistance, as was high expression of cell cycle gene signatures after treatment.

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Pancreatic carcinoma and Colon carcinoma tissue ar Breast carcinoma tissue a Cervix carcinoma for anti Esophageal squamous cell Small cell lung carcinoma Liver carcinoma and norma Colon carcinoma tissue ar Multi organ carcinoma tis Digestive system carcinom Normal liver and hepatoce Non small cell lung carci

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Comprehensive Assessment of GPR68 Expression in Normal and Neoplastic Human Tissues Using a Novel Rabbit Monoclonal Antibody.

GPR68 (OGR1) belongs to the proton-sensing G protein-coupled receptors that are involved in cellular adaptations to pH changes during tumour development. Although expression of GPR68 has been described in many tumour cell lines, little is known about its presence in human tumour entities. We characterised the novel rabbit monoclonal anti-human GPR68 antibody 16H23L16 using various cell lines and tissue specimens. The antibody was then applied to a large series of formalin-fixed, paraffin-embedded normal and neoplastic human tissue samples. Antibody specificity was demonstrated in a Western blot analysis of GPR68-expressing cells using specific siRNAs. Immunocytochemical experiments revealed pH-dependent changes in subcellular localisation of the receptor and internalisation after stimulation with lorazepam. In normal tissue, GPR68 was present in glucagon-producing islet cells, neuroendocrine cells of the intestinal tract, gastric glands, granulocytes, macrophages, muscle layers of arteries and arterioles, and capillaries. GPR68 was also expressed in neuroendocrine tumours, where it may be a positive prognostic factor, in pheochromocytomas, cervical adenocarcinomas, and endometrial cancer, as well as in paragangliomas, medullary thyroid carcinomas, gastrointestinal stromal tumours, and pancreatic adenocarcinomas. Often, tumour capillaries were also strongly GPR68-positive. The novel antibody 16H23L16 will be a valuable tool for basic research and for identifying GPR68-expressing tumours during histopathological examinations.

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MID1 interacting G12-like Inhibin beta-A antibody S Proteasome inhibitor PI31 Protease Inhibitor 15 ant Integrin β1 (CD29) Antib Anti AGO2 Human, Monoclon INPP1 antibody Source Rab Rabbit Anti-TNIP2 ABIN2 T Interleukin-24 antibody S Inhibitory Monoclonal ant Interferon alpha-8 antibo Rabbit Anti-Cell death in

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Pembrolizumab-induced necrotizing myositis in a patient with metastatic non-small-cell lung cancer: a case report.

A 57-year-old man presented with swelling and pain in the lower limbs, inability to walk and increasing dyspnea for 2 days. Because of refractory stage IV non-small-cell lung cancer, pembrolizumab was started 21 days before presentation. Since then, he experienced general discomfort, fatigue and bilateral weakness in the legs with exercise limitation. A diagnosis of pembrolizumab-induced grade III myositis was made based on muscle biopsy. Pembrolizumab is a humanized monoclonal antibody against PD-1. It has been approved for the treatment of metastatic melanoma and refractory non-small-cell lung cancer with increased expression of PD-L1 on the cell surface of tumor cells. With such a humanized monoclonal antibody, fewer adverse events are expected than with systemic chemotherapy. However, 13% of patients develop autoimmune side effects which can be severe (grade III, IV or V) in 5-10%. We discuss a case of pembrolizumab-induced myositis, with a brief overview of the literature. Only three cases of pembrolizumab-induced myositis have been reported in literature.

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