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Search results for: Anti-bodywall muscle cells Monoclonal Antibody


#32614850   2020/07/02 To Up

Brain-specific angiogenesis inhibitor 1 is expressed in the Myo/Nog cell lineage.

The Myo/Nog cell lineage was discovered in the chick embryo and is also present in adult mammalian tissues. The cells are named for their expression of mRNA for the skeletal muscle specific transcription factor MyoD and bone morphogenetic protein inhibitor Noggin. A third marker for Myo/Nog cells is the cell surface molecule recognized by the G8 monoclonal antibody (mAb). G8 has been used to detect, track, isolate and kill Myo/Nog cells. In this study, we screened a membrane proteome array for the target of the G8 mAb. The array consisted of >5,000 molecules, each synthesized in their native confirmation with appropriate post-translational modifications in a single clone of HEK-293T cells. G8 mAb binding to the clone expressing brain-specific angiogenesis inhibitor 1 (BAI1) was detected by flow cytometry, re-verified by sequencing and validated by transfection with the plasmid construct for BAI1. Further validation of the G8 target was provided by enzyme-linked immunosorbent assay. The G8 epitope was identified by screening a high-throughput, site directed mutagenesis library designed to cover 95-100% of the 954 amino acids of the extracellular domain of the BAI1 protein. The G8 mAb binds within the third thrombospondin repeat of the extracellular domain of human BAI1. Immunofluorescence localization experiments revealed that G8 and a commercially available BAI1 mAb co-localize to the subpopulation of Myo/Nog cells in the skin, eyes and brain. Expression of the multi-functional BAI1 protein in Myo/Nog cells introduces new possibilities for the roles of Myo/Nog cells in normal and diseased tissues.
Jacquelyn Gerhart, Jessica Bowers, Lindsay Gugerty, Colby Gerhart, Mark Martin, Fathma Abdalla, Arturo Bravo-Nuevo, Jonathan Tabb Sullivan, Rebecca Rimkunas, Amie Albertus, Lou Casta, Lori Getts, Robert Getts, Mindy George-Weinstein

1242 related Products with: Brain-specific angiogenesis inhibitor 1 is expressed in the Myo/Nog cell lineage.

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#32536096   // To Up

[Analysis of clinicopathological features of clear cell tumor of the lung].

To analyze the clinicopathological features of clear cell tumor of the lung (CCTL). A total of 9 cases were collected from August 2008 to August 2019 in the Department of Pathology of the First Medical Center of PLA General Hospital and Hainan Hospital of PLA General Hospital. Their clinical data, pathological characteristics, immunohistochemical staining and special staining results were summarized and analyzed. There were 3 males and 6 females, aged from 28 to 70 years (average 52.2 years). All tumors were located in the peripheral part of the lung, and were solitary in 8 cases, and multiple (24 nodules) in 1 case. The lesion was round or oval, with clear boundary. The diameter of the nodule was 0.5-5.5 cm. Histologically, the tumor cells were oval, short fusiform or polygonal, with obvious nucleoli. The tumor cells were mostly distributed in sheet around thin-walled vessels, and there was hyaline degeneration around the blood vessels. Neither necrosis nor mitosis could be seen. Immunohistochemical staining showed tumor cells were diffusely positive for Vimentin, and CD34, Melan-A, specific monoclonal antibody against melanoma (HMB45) and S-100 were positive with different degrees. Broad spectrum cytokeratin (CK), epithelial membrane antigen (EMA), smooth muscle actin (SMA), desmin, CD10, paired box gene 8 (PAX-8) or myomodulatory protein (Myo-D1) were all negative. The positive index of the proliferating cell nuclear antigen (Ki-67) was low. Schiff dyeing with periodate (PAS) staining was positive, PAS staining of glycogen digested by amylase (d-PAS) staining was negative. All the tumors in the nine cases were resected and patients were followed up for 5-137 months. Except 1 case was lost for follow-up, the other 8 cases survived without recurrence or metastasis of the disease. CCTL is a rare benign tumor, most of which are single, few of which can be multiple; histopathological characteristics and immunohistochemical staining are helpful for diagnosis and differentiated diagnosis. After complete resection, the prognosis was good. However, when histological features indicating malignancy, intense follow-up should be considered.
Y Liu, X H Zhang, B T Wang, L L Shen, J Yuan, W Chen, J Gao, H Y Shi

1525 related Products with: [Analysis of clinicopathological features of clear cell tumor of the lung].

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#32523455   2020/03/23 To Up

Coronary inflammation: why searching, how to identify and treat it.

Inflammation plays an important role in the development of atherosclerotic lesions. A variety of stimuli promote atherosclerosis, including increased LDL cholesterol in blood, exposure to tobacco, diabetes mellitus, hypertension, or rheological stress. Inflammatory cells have an established role in the growth of atherosclerotic lesions. Macrophages recognize and internalise ox-LDL to eventually become lipid-laden foam cells, the hallmark cellular component of atheroma. Infiltrating CD4-T cells have a role too, by interacting with ox-LDL and other antigens. Cytokines secreted by inflammatory cells stimulate smooth muscle cells migration whilst macrophages produce metalloprotease that lead to fibrous cap rupture. The necrotic debris of died macrophages and smooth muscle cells help to continue the inflammatory process. The inflammatory response can also directly activate platelets and promote thrombus formation at the surface of complicated coronary plaques. The CANTOS trial can be waived as an innovative study promoting a novel approach of personalized medicine. In patients with previous myocardial infarction, high-sensitivity C-reactive protein level of 2 mg and normal LDL level (<70 mg/dL), canakinumab a therapeutic monoclonal antibody targeting interleukin-1β, at a dose of 150 mg every 3 months, led to a significant reduction of the primary efficacy end point: nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death at 48 months. Based on the CANTOS results, patients on statins and residual inflammatory risk as assessed by means of a high-sensitivity CRP >2 mg/l at baseline have a high risk of future cardiac events, comparable to that of statin-treated patients with suboptimal cholesterol LDL level. The inhibition of interleukin-1β by means of canakinumab, which is only one of many potential anti-inflammatory pathways, open new perspectives, showing that a selective inhibition of the inflammatory pathway may be beneficial in reducing cardiovascular risk. In a process of personalized medicine, there is need to accurately identify patients at high risk of events, to be treated with potent statins or anti-inflammatory drugs. Perhaps in the near future a more specific assessment of coronary inflammations, possibly obtained with imaging modalities (either invasive or non-invasive), will better select patients at risk of events. In this scenario, in the setting of secondary prevention, OCT may serve the scope of identifying vulnerable plaques with local aggregates of inflammatory cells. Future studies are needed to understand the clinical effectiveness of strategies based on invasive coronary assessment.
Francesco Prati, Valeria Marco, Giulia Paoletti, Mario Albertucci

1414 related Products with: Coronary inflammation: why searching, how to identify and treat it.

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#32500296   2020/06/04 To Up

Research Progress on the Involvement of ANGPTL4 and Loss-of-Function Variants in Lipid Metabolism and Coronary Heart Disease: Is the "Prime Time" of ANGPTL4-Targeted Therapy for Coronary Heart Disease Approaching?

Multiple genetic studies have confirmed the definitive link among the loss-of-function variants of angiogenin-like protein 4 (ANGPTL4), significantly decreased plasma triglyceride (TG) levels, and reduced risk of coronary heart disease (CHD). The potential therapeutic effect of ANGPTL4 on dyslipidemia and CHD has been widely studied.
Jingmin Yang, Xiao Li, Danyan Xu

2884 related Products with: Research Progress on the Involvement of ANGPTL4 and Loss-of-Function Variants in Lipid Metabolism and Coronary Heart Disease: Is the "Prime Time" of ANGPTL4-Targeted Therapy for Coronary Heart Disease Approaching?

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#32431692   2020/05/05 To Up

Long-Lasting Rituximab-Induced Reduction of Specific-But Not Total-IgG4 in MuSK-Positive Myasthenia Gravis.

The use of rituximab (RTX), an anti-CD20 monoclonal antibody (Ab), in refractory myasthenia gravis (MG) is associated with a better response in patients with Abs to the muscle-specific tyrosine kinase (MuSK) than in other MG subgroups. Anti-MuSK Abs are mostly IgG4 with proven pathogenicity and positive correlation with clinical severity. The rapid and sustained response to RTX may be related to MuSK Ab production by short-lived Ab-secreting cells derived from specific CD20 B cells. Here, we investigated the long-term effects of RTX in nine refractory MuSK-MG patients with a follow-up ranging from 17 months to 13 years. In patients' sera, we titrated MuSK-specific IgG (MuSK-IgG) and MuSK-IgG4, along with total IgG and IgG4 levels. Optimal response to RTX was defined as the achievement and maintenance of the status of minimal manifestations (MM)-or-better together with ≥ 50% steroid reduction, withdrawal of immunosuppressants, and no need for plasma-exchange or intravenous immunoglobulin. After a course of RTX, eight patients improved, with optimal response in six, while only one patient did not respond. At baseline, MuSK-IgG and MuSK-IgG4 serum titers were positive in all patients, ranging from 2.15 to 49.5 nmol/L and from 0.33 to 46.2 nmol/L, respectively. MuSK Abs mostly consisted of IgG4 (range 63.80-98.86%). RTX administration was followed by a marked reduction of MuSK Abs at 2-7 months and at 12-30 months ( < 0.02 for MuSK-IgG and < 0.01 for MuSK-IgG4). In patients with a longer follow-up, MuSK Ab titers remained suppressed, paralleling clinical response. In the patient who achieved long-term complete remission, MuSK-IgG4 was no longer detectable within 2 years, while MuSK-IgG remained positive at very low titers up to 10 years after RTX. In the patient who did not respond, MuSK-IgG and MuSK-IgG4 remained unchanged. In this patient series, total IgG and IgG4 transiently decreased ( < 0.05) at 2-7 months after RTX. The different trends of reduction between MuSK-IgG4 and total IgG4 after RTX support the view that short-lived Ab-secreting cells are the main producers of MuSK Abs. The ratio between short-lived Ab-secreting cells and long-lived plasma cells may influence the response to RTX, and B-cell severe depletion may reduce self-maintaining autoimmune reactivity.
Mariapaola Marino, Umberto Basile, Gregorio Spagni, Cecilia Napodano, Raffaele Iorio, Francesca Gulli, Laura Todi, Carlo Provenzano, Emanuela Bartoccioni, Amelia Evoli

1256 related Products with: Long-Lasting Rituximab-Induced Reduction of Specific-But Not Total-IgG4 in MuSK-Positive Myasthenia Gravis.

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#32427867   2020/05/19 To Up

Comparative analysis of MACROD1, MACROD2 and TARG1 expression, localisation and interactome.

The posttranslational modification ADP-ribosylation is involved in many cellular processes, with distinct roles for poly- and mono(ADP-ribosyl)ation (PAR- and MARylation, respectively). Reversibility of intracellular MARylation was demonstrated with the discovery of MACROD1, MACROD2 and TARG1, three macrodomain-containing enzymes capable of reversing MARylation of proteins and RNA. While the three enzymes have identical activities in vitro, their roles in cells are unclear and published data are partially contradictory, possibly due to a lack of validated reagents. We developed monoclonal antibodies to study these proteins and analysed their tissue distribution and intracellular localisation. MACROD1 is most prevalent in mitochondria of skeletal muscle, MACROD2 localises to nucleo- and cytoplasm and is found so far only in neuroblastoma cells, whereas the more ubiquitously expressed TARG1 is present in nucleoplasm, nucleolus and stress granules. Loss of MACROD1 or loss of TARG1 leads to disruption of mitochondrial or nucleolar morphology, respectively, hinting at their importance for these organelles. To start elucidating the underlying mechanisms, we have mapped their interactomes using BioID. The cellular localisation of interactors supports the mitochondrial, nucleolar and stress granule localisation of MACROD1 and TARG1, respectively. Gene ontology analysis suggests an involvement of MACROD1 and TARG1 in RNA metabolism in their respective compartments. The detailed description of the hydrolases' expression, localisation and interactome presented here provides a solid basis for future work addressing their physiological function in more detail.
R Žaja, G Aydin, B E Lippok, R Feederle, B Lüscher, K L H Feijs

2971 related Products with: Comparative analysis of MACROD1, MACROD2 and TARG1 expression, localisation and interactome.

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#32362501   2020/04/30 To Up

Antibodies in cerebral cavernous malformations react with cytoskeleton autoantigens in the lesional milieu.

Previous studies have reported robust inflammatory cell infiltration, synthesis of IgG, B-cell clonal expansion, deposition of immune complexes and complement within cerebral cavernous malformation (CCM) lesions. B-cell depletion has also been shown to reduce the maturation of CCM in murine models. We hypothesize that antigen(s) within the lesional milieu perpetuate the pathogenetic immune responses in CCMs. This study aims to identify those putative antigen(s) using monoclonal antibodies (mAbs) derived from plasma cells found in surgically removed human CCM lesions. We produced human mAbs from laser capture micro-dissected plasma cells from four CCM patients, and also germline-reverted versions. CCM mAbs were assayed using immunofluorescence on central nervous system (CNS) tissues and immunocytochemistry on human primary cell lines. Antigen characterization was performed using a combination of confocal microscopy, immunoprecipitation and mass spectrometry. Affinity was determined by enzyme-linked immunosorbent assay, and specificity by multi-color confocal microscopy and quantitative co-localization. CCM mAbs bound CNS tissue, especially endothelial cells and astrocytes. Non-muscle myosin heavy chain IIA (NMMHCIIA), vimentin and tubulin are three cytoskeleton proteins that were commonly targeted. Selection of cytoskeleton proteins by plasma cells was supported by a high frequency of immunoglobulin variable region somatic hypermutations, high affinity and selectivity of mAbs in their affinity matured forms, and profoundly reduced affinity and selectivity in the germline reverted forms. Antibodies produced by plasma cells in CCM lesions commonly target cytoplasmic and cytoskeletal autoantigens including NMMHCIIA, vimentin and tubulin that are abundant in endothelial cells and astrocytes. Binding to, and selection on autoantigen(s) in the lesional milieu likely perpetuates the pathogenetic immune response in CCMs. Blocking this in situ autoimmune response may yield a novel treatment for CCM.
Dongdong Zhang, Andrew J Kinloch, Abhinav Srinath, Robert Shenkar, Romuald Girard, Rhonda Lightle, Thomas Moore, Janne Koskimäki, Azam Mohsin, Julián Carrión-Penagos, Sharbel Romanos, Le Shen, Marcus R Clark, Changbin Shi, Issam A Awad

1066 related Products with: Antibodies in cerebral cavernous malformations react with cytoskeleton autoantigens in the lesional milieu.

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#32270492   2020/04/09 To Up

Selective inhibition of anti-MAG IgM autoantibody binding to myelin by an antigen-specific glycopolymer.

Anti-myelin-associated glycoprotein (MAG) neuropathy is a disabling autoimmune peripheral neuropathy that is caused by circulating monoclonal IgM autoantibodies directed against the human natural killer-1 (HNK-1) epitope. This carbohydrate epitope is highly expressed on adhesion molecules such as MAG, a glycoprotein present in myelinated nerves. We previously showed the therapeutic potential of the glycopolymer poly(phenyl disodium 3-O-sulfo-β-d-glucopyranuronate)-(1→3)-β-d-galactopyranoside (PPSGG) in selectively neutralizing anti-MAG IgM antibodies in an immunological mouse model and ex vivo with sera from anti-MAG neuropathy patients. PPSGG is composed of a biodegradable backbone that multivalently presents a mimetic of the HNK-1 epitope. In this study, we further explored the pharmacodynamic properties of the glycopolymer and its ability to inhibit the binding of anti-MAG IgM to peripheral nerves. The polymer selectively bound anti-MAG IgM autoantibodies and prevented the binding of patients' anti-MAG IgM antibodies to myelin of non-human primate sciatic nerves. Upon PPSGG treatment, neither activation nor inhibition of human and murine peripheral blood mononuclear cells nor alteration of systemic inflammatory markers was observed in mice or ex vivo in human peripheral blood mononuclear cells. Intravenous injections of PPSGG to mice immunized against the HNK-1 epitope removed anti-MAG IgM antibodies within less than 1 hr, indicating a fast and efficient mechanism of action as compared to a B-cell depletion with anti-CD20. In conclusion, these observations corroborate the therapeutic potential of PPSGG for an antigen-specific treatment of anti-MAG neuropathy.
Butrint Aliu, Delphine Demeestere, Emilie Seydoux, José Boucraut, Emilien Delmont, Alexandre Brodovitch, Thomas Oberholzer, Shahram Attarian, Marie Théaudin, Pinelopi Tsouni, Thierry Kuntzer, Tobias Derfuss, Andreas J Steck, Beat Ernst, Ruben Herrendorff, Pascal Hänggi

1178 related Products with: Selective inhibition of anti-MAG IgM autoantibody binding to myelin by an antigen-specific glycopolymer.

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#32250537   2020/04/20 To Up

Perisynaptic Schwann cells phagocytose nerve terminal debris in a mouse model of Guillain-Barré syndrome.

In mouse models of acute motor axonal neuropathy, anti-ganglioside antibodies (AGAbs) bind to motor axons, notably the distal nerve, and activate the complement cascade. While complement activation is well studied in this model, the role of inflammatory cells is unknown. Herein we aimed to investigate the contribution of phagocytic cells including macrophages, neutrophils and perisynaptic Schwann cells (pSCs) to distal nerve pathology. To observe this, we first created a subacute injury model of sufficient duration to allow inflammatory cell recruitment. Mice were injected intraperitoneally with an anti-GD1b monoclonal antibody that binds strongly to mouse motor nerve axons. Subsequently, mice received normal human serum as a source of complement. Dosing was titrated to allow humane survival of mice over a period of 3 days, yet still induce the characteristic neurological impairment. Behaviour and pathology were assessed in vivo using whole-body plethysmography and post-sacrifice by immunofluorescence and flow cytometry. ex vivo nerve-muscle preparations were used to investigate the acute phagocytic role of pSCs following distal nerve injury. Following complement activation at distal intramuscular nerve sites in the diaphragm macrophage localisation or numbers are not altered, nor do they shift to a pro- or anti-inflammatory phenotype. Similarly, neutrophils are not significantly recruited. Instead, ex vivo nerve-muscle preparations exposed to AGAb plus complement reveal that pSCs rapidly become phagocytic and engulf axonal debris. These data suggest that pSCs, rather than inflammatory cells, are the major cellular vehicle for axonal debris clearance following distal nerve injury, in contrast to larger nerve bundles where macrophage-mediated clearance predominates.
Madeleine E Cunningham, Gavin R Meehan, Sophie Robinson, Denggao Yao, Rhona McGonigal, Hugh J Willison

2463 related Products with: Perisynaptic Schwann cells phagocytose nerve terminal debris in a mouse model of Guillain-Barré syndrome.

2 ml100 μg0.5 mg10100.00 ug4 Arrays/Slide100.00 ug100 ul1.00 flask200 25 TESTS1mg

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#32233931   2020/04/01 To Up

Characterization of a Novel Interleukin-1 Receptor Antagonist from Sheep ().

Interleukin-1 receptor antagonist (IL-1Ra) is an antagonist of IL-1β binding IL-1β receptors but does not induce intracellular responses or signal transduction. In this study, the full-length complementary DNA (cDNA) of the gene () was identified from sheep () using rapid amplification of cDNA ends PCR and submitted to GenBank with the accession number KC425613. The cDNA comprised an open reading frame of 525 bp encoding a protein of 19765.8 Da, a 5'-untranslated region (UTR) of 27 bp, and a 3'-UTR of 676 bp with a poly(A) tail. Recombinant OaIL-1Ra with bioactivity was expressed in a prokaryotic expression system, and a monoclonal antibody against native OaIL-1Ra was prepared. Through Western blot analyses, the OaIL-1Ra protein was widely expressed in lung, heart, spleen, liver, kidney, muscle, intestine, lymphonodi, rumen, and white blood cells, with the highest levels in liver and spleen. The expression of OaIL-1Ra in primary cultured white blood cells of sheep were highly induced in a time-dependent manner when challenged with different bacteria. These results implied that is associated with immune responses during bacterial infections.
Shi-Jun Zhang, Xing Guo, Pan Hu, Shi-Ying Lu, Nan-Nan Liu, Bao-Quan Fu, Nan Wang, Yan-Song Li, Lu-Lu Wang, Jiang Chang, Heng-Zhen Chang, Zeng-Shan Liu, Yu Zhou, Hong-Lin Ren

1891 related Products with: Characterization of a Novel Interleukin-1 Receptor Antagonist from Sheep ().

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