Mouse IgM (µ) (min X Hu Ig, Ch,Rab,Gt,Sh,Bov,Hrs,Dg,Sw,Bab IgG), Clone LOMM9, Rat Mab anti_, Biotin

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891 EUR
1069 USD
739 GBP
known as: Mouse IgM (µ) (min X Hu Ig, Ch,Rab,Gt,Sh,Bov,Hrs,Dg,Sw,Bab IgG), Clone LOMM9, Rat Mab anti_, Biotin
Catalog number: genta-YULLOMM9-B1
Product Quantity: 1 ml.
Category:
Supplier: Accu

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Gene target: min x hu ig ch rab gt sh bov hrs dg sw bab clone lomm9 mab

Related genes to: Mouse IgM (µ) (min X Hu Ig, Ch,Rab,Gt,Sh,Bov,Hrs,Dg,Sw,Bab IgG), Clone LOMM9, Rat Mab anti_, Biotin

Symbol : biotin NIH gene
LocusTag : Bathy11g00270
chromosome : 11
description : biotin synthase
type of gene : protein-coding
Modification date : 2015-06-26
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 : IGM NIH gene
description : IgM constant region
type of gene : other
Modification date : 2016-04-02
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
Symbol : rab NIH gene
description : rab protein
type of gene : protein-coding
Modification date : 2015-11-14

Related Pathways to: Mouse IgM (µ) (min X Hu Ig, Ch,Rab,Gt,Sh,Bov,Hrs,Dg,Sw,Bab IgG), Clone LOMM9, Rat Mab anti_, Biotin

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Related product to: Mouse IgM (µ) (min X Hu Ig, Ch,Rab,Gt,Sh,Bov,Hrs,Dg,Sw,Bab IgG), Clone LOMM9, Rat Mab anti_, Biotin

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Related Articles about: Mouse IgM (µ) (min X Hu Ig, Ch,Rab,Gt,Sh,Bov,Hrs,Dg,Sw,Bab IgG), Clone LOMM9, Rat Mab anti_, Biotin

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

Analysis of K-Ras Interactions by Biotin Ligase Tagging.

Mutations of the human K-Ras 4B (K-Ras) G protein are associated with a significant proportion of all human cancers. Despite this fact, a comprehensive analysis of K-Ras interactions is lacking. Our investigations focus on characterization of the K-Ras interaction network. - Source :PubMed

Specific IgM and Regulation of Antibody Responses.

Specific IgM, administered together with the antigen it recognizes, enhances primary antibody responses, formation of germinal centers, and priming for secondary antibody responses. The response to all epitopes on the antigen to which IgM binds is usually enhanced. IgM preferentially enhances responses to large antigens such as erythrocytes, malaria parasites, and keyhole limpet hemocyanine. In order for an effect to be seen, antigens must be administered in suboptimal concentrations and in close temporal relationship to the IgM. Enhancement is dependent on the ability of IgM to activate complement, but the lytic pathway is not required. Enhancement does not take place in mice lacking complement receptors 1 and 2 (CR1/2) suggesting that the role of IgM is to generate C3 split products, i.e., the ligands for CR1/2. In mice, these receptors are expressed on follicular dendritic cells (FDCs) and B cells. Optimal IgM-mediated enhancement requires that both cell types express CR1/2, but intermediate enhancement is seen when only FDCs express the receptors and low enhancement when only B cells express them. These observations imply that IgM-mediated enhancement works through several, non-mutually exclusive, pathways. Marginal zone B cells can transport IgM-antigen-complement complexes, bound to CR1/2, from the marginal zone and deposit them onto FDCs. In addition, co-crosslinking of the BCR and the CR2/CD19/CD81 co-receptor complex may enhance signaling to specific B cells, a mechanism likely to be involved in induction of early extrafollicular antibody responses. - Source :PubMed

Rab Interacting Molecules 2 and 3 Directly Interact with the Pore-Forming CaV1.3 Ca(2+) Channel Subunit and Promote Its Membrane Expression.

Rab interacting molecules (RIMs) are multi-domain proteins that positively regulate the number of Ca(2+) channels at the presynaptic active zone (AZ). Several molecular mechanisms have been demonstrated for RIM-binding to components of the presynaptic Ca(2+) channel complex, the key signaling element at the AZ. Here, we report an interaction of the C2B domain of RIM2α and RIM3γ with the C-terminus of the pore-forming α-subunit of CaV1.3 channels (CaV1.3α1), which mediate stimulus-secretion coupling at the ribbon synapses of cochlear inner hair cells (IHCs). Co-expressing full-length RIM2α with a Ca(2+) channel complex closely resembling that of IHCs (CaV1.3α1-CaVß2a) in HEK293 cells doubled the Ca(2+)-current and shifted the voltage-dependence of Ca(2+) channel activation by approximately +3 mV. Co-expression of the short RIM isoform RIM3γ increased the CaV1.3α1-CaVß2a-mediated Ca(2+)-influx in HEK293 cells, but disruption of RIM3γ in mice left Ca(2+)-influx in IHCs and hearing intact. In conclusion, we propose that RIM2α and RIM3γ directly interact with the C-terminus of the pore-forming subunit of CaV1.3 Ca(2+) channels and positively regulate their plasma membrane expression in HEK293 cells. - Source :PubMed

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