Mouse IgG2a (min X Ck,Rb,Gt,Hrs,Sw,Bab,Hu IgG, Hu IgM), Clone LOMG2a2, Rat Mab anti_, HRP

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known as: Mouse IgG2a (min X Ck,Rb,Gt,Hrs,Sw,Bab,Hu IgG, Hu IgM), Clone LOMG2a2, Rat Mab anti_, HRP
Catalog number: genta-YULLOMG2a2-P05
Product Quantity: 0.5 ml.
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Supplier: Accu

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Gene target: igg2a min x ck rb gt hrs sw bab hu clone lomg2a2 mab

Related genes to: Mouse IgG2a (min X Ck,Rb,Gt,Hrs,Sw,Bab,Hu IgG, Hu IgM), Clone LOMG2a2, Rat Mab anti_, HRP

Symbol : Hrs NIH gene
LocusTag : Dmel_CG2903
Synonyms : CG2903|DmHRS|DmelCG2903|HRS|HRS-2|Vps27|dHrs|hrs|l(2)23AB5|l(2)23Ad|l(2)23Ad(Hrs)|vps27
dbXrefs : FLYBASE:FBgn0031450
chromosome : 2L
map location : 23A3-23A3
description : Hepatocyte growth factor regulated tyrosine kinase substrate
type of gene : protein-coding
Symbol from nomenclature authority : Hrs
Full name from nomenclature authority : Hepatocyte growth factor regulated tyrosine kinase substrate
Nomenclature status : O
Other designations : CG2903-PA|CG2903-PB|CG2903-PC|F[[1]]F[[0]] ATPase|HGF-regulated tyrosine kinase substrate|Hrs-PA|Hrs-PB|Hrs-PC|hepatocyte growth factor regulated tyrosine kinase|hepatocyte growth factor regulated tyrosine kinase substrate|hepatocyte growth factor-re
Modification date : 2016-06-11
Symbol : IGG NIH gene
dbXrefs : AnimalQTLdb:17939
chromosome : 2
map location : 2 0.2 cM
description : Immunoglobulin G level
type of gene : unknown
Modification date : 2015-01-24
Symbol : min NIH gene
Synonyms : mi
dbXrefs : FLYBASE:FBgn0002747
chromosome : 2
map location : 56E-56E|2-90 cM
description : mini
type of gene : unknown
Modification date : 2016-05-09

Related Pathways to: Mouse IgG2a (min X Ck,Rb,Gt,Hrs,Sw,Bab,Hu IgG, Hu IgM), Clone LOMG2a2, Rat Mab anti_, HRP

Gene about :IgG
Pathway :Mm Microglia Pathogen Phagocytosis Pathway
IgG

Related product to: Mouse IgG2a (min X Ck,Rb,Gt,Hrs,Sw,Bab,Hu IgG, Hu IgM), Clone LOMG2a2, Rat Mab anti_, HRP

Related Articles about: Mouse IgG2a (min X Ck,Rb,Gt,Hrs,Sw,Bab,Hu IgG, Hu IgM), Clone LOMG2a2, Rat Mab anti_, HRP

MinE conformational dynamics regulate membrane binding, MinD interaction, and Min oscillation.

In Escherichia coli MinE induces MinC/MinD to oscillate between the ends of the cell, contributing to the precise placement of the Z ring at midcell. To do this, MinE undergoes a remarkable conformational change from a latent 6β-stranded form that diffuses in the cytoplasm to an active 4β-stranded form bound to the membrane and MinD. How this conformational switch occurs is not known. Here, using hydrogen-deuterium exchange coupled to mass spectrometry (HDX-MS) we rule out a model in which the two forms are in rapid equilibrium. Furthermore, HDX-MS revealed that a MinE mutant (D45A/V49A), previously shown to produce an aberrant oscillation and unable to assemble a MinE ring, is more rigid than WT MinE. This mutant has a defect in interaction with MinD, suggesting it has difficulty in switching to the active form. Analysis of intragenic suppressors of this mutant suggests it has difficulty in releasing the N-terminal membrane targeting sequences (MTS). These results indicate that the dynamic association of the MTS with the β-sheet is fine-tuned to balance MinE's need to sense MinD on the membrane with its need to diffuse in the cytoplasm, both of which are necessary for the oscillation. The results lead to models for MinE activation and MinE ring formation. - Source :PubMed

Construction of a Recombinant Full-length Membrane Associated IgG Library.

HIV/AIDS has become a global pandemic. Development of an effective HIV-1 vaccine eliciting broadly neutralizing monoclonal antibodies (bnmAbs) remains a big challenge. Before an effective vaccine comes out, passive treatment for prevention and protection of HIV-1 infection may alleviate the burden caused by the pandemic. Numerous bnmAbs have been isolated against different epitopes in HIV-1 envelope glycoprotein via phage/yeast display, EBV-immortalization, single cell sorting and micro neutralization. Recombinant antibody library with extended diversity and enlarged size of units are applicable by phage/yeast display and mammalian cell display for monoclonal antibody isolation. Here, we constructed an immune recombinant membrane associated full length IgGs library based on mammalian cell display system. This library can be used for monoclonal antibody screening/isolation by target cell sorting. A full length antibody mz2F11 was screened with potent neutralizing activities against a panel of viruses tested. Our study provides a novel way of antibody library construction and monoclonal antibody screening. Antibodies screened via this method can help broaden the knowledge in passive treatment and prevention against HIV-1 infection. - Source :PubMed

Chronic Trichuris muris infection causes neoplastic change in the intestine and exacerbates tumour formation in APC min/+ mice.

Incidences of infection-related cancers are on the rise in developing countries where the prevalence of intestinal nematode worm infections are also high. Trichuris muris (T. muris) is a murine gut-dwelling nematode that is the direct model for human T. trichiura, one of the major soil-transmitted helminth infections of humans. In order to assess whether chronic infection with T. muris does indeed influence the development of cancer hallmarks, both wild type mice and colon cancer model (APC min/+) mice were infected with this parasite. Parasite infection in wild type mice led to the development of neoplastic change similar to that seen in mice that had been treated with the carcinogen azoxymethane. Additionally, both chronic and acute infection in the APCmin/+ mice led to an enhanced tumour development that was distinct to the site of infection suggesting systemic control. By blocking the parasite specific T regulatory response in these mice, the increase in the number of tumours following infection was abrogated. Thus T. muris infection alone causes an increase in gut pathologies that are known to be markers of cancer but also increases the incidence of tumour formation in a colon cancer model. The influence of parasitic worm infection on the development of cancer may therefore be significant. - Source :PubMed

Point-of-care testing for Toxoplasma gondii IgG/IgM using Toxoplasma ICT IgG-IgM test with sera from the United States and implications for developing countries.

Congenital toxoplasmosis is a serious but preventable and treatable disease. Gestational screening facilitates early detection and treatment of primary acquisition. Thus, fetal infection can be promptly diagnosed and treated and outcomes can be improved. - Source :PubMed

High dose IVIG successfully reduces high rhGAA IgG antibody titers in a CRIM-negative infantile Pompe disease patient.

Alglucosidase alfa (rhGAA) has altered the course of an otherwise fatal outcome in classic infantile Pompe disease (IPD), which presents with cardiomyopathy and severe musculoskeletal involvement. However, the response to therapy is determined by several factors including the development of high and sustained antibody titers (HSAT) to rhGAA. Cross-reactive immunologic material (CRIM) negative patients are at the highest risk for development of HSAT. Immune tolerance induction (ITI) with methotrexate, rituximab, and intravenous immunoglobulin (IVIG) has been largely successful in preventing the immune response and in achieving tolerance when done in conjunction with enzyme replacement therapy (ERT) initiation. Reducing antibody titers in cases with an entrenched immune response remains a challenge in the field despite the use of multiple immunomodulatory agents. Success has been shown with addition of bortezomib to the ITI regimen, yet the prolonged course and potential risks with the use of such agents' demands caution. We present here a 7-year-old CRIM-negative IPD patient who was not successfully tolerized by an ITI regimen with rituximab, methotrexate, and IVIG due to intolerability to the regimen and recurrent infections. She went on to develop HSAT, with significant clinical decline, loss of all motor abilities, and a fragile medical state, which made it challenging to institute the bortezomib based regimen to reduce HSAT. She had severe developmental delay, respiratory failure with invasive ventilation and tracheostomy, persistent hypotonia, ptosis of eyelids, diffuse severe osteopenia, contractures, and was completely G-tube fed. As a rescue mechanism, we treated her with high dose and high frequency IVIG in an attempt to reduce rhGAA IgG antibody titers (antibody titers; titers). Her titers saw a steady decline on weekly IVIG doses at 1g/kg for 20weeks. Subsequently when the IVIG regimen was altered to 1g/kg every month, rising titers were detected and therefore the regimen was changed to a biweekly regimen. High dose IVIG resulted in an eightfold decrease in antibody titers. Clinically, she showed improvement with partial recovery of previously lost motor abilities, especially hand movements and better head and neck control than before. The regimen was safely tolerated with no hospitalizations. The effectiveness of IVIG as a single agent, in this case with multiple comorbidities and fragile clinical status, was lifesaving and may represent an effective, perhaps lifesaving rescue approach to reduce antibody titers. - Source :PubMed

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