Mouse IgM (µ) (min X Hu, Bov, Hrs, Rat Sr Prot), Texas Red

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607 EUR
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503 GBP
known as: Mouse IgM (µ) (min X Hu, Bov, Hrs, Rat Sr Prot), Texas Red
Catalog number: genta-JNM075140
Product Quantity: 0.5 mg.
Category:
Supplier: Accu

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Gene target: min x hu bov hrs sr prot red

Related genes to: Mouse IgM (µ) (min X Hu, Bov, Hrs, Rat Sr Prot), Texas Red

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 : Prot NIH gene
dbXrefs : MGI:MGI:107578
chromosome : 18
description : proline transporter
type of gene : protein-coding
Symbol from nomenclature authority : Prot
Full name from nomenclature authority : proline transporter
Nomenclature status : O
Modification date : 2016-07-02

Related Pathways to: Mouse IgM (µ) (min X Hu, Bov, Hrs, Rat Sr Prot), Texas Red

Gene about :IgM
Pathway :Rn Inflammatory Response Pathway
IgM

Related product to: Mouse IgM (µ) (min X Hu, Bov, Hrs, Rat Sr Prot), Texas Red

Related Articles about: Mouse IgM (µ) (min X Hu, Bov, Hrs, Rat Sr Prot), Texas Red

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

Development and evaluation of polyclonal antisera for detection of the IgM heavy chain of multiple fish species.

Antibodies are widely considered to be essential tools for detection of immune responses in various fish species. Here we produced the peptide polyclonal antisera (anti-fish IgH-1 and anti-fish IgH-2) to detect IgM of various fish species. The peptides were designed based on the conserved sequence of the fish immunoglobulin heavy chains of seven fish species (Japanese flounder, seabream, yellowtail, carp, rainbow trout, hybrid sturgeon and banded houndshark). By Western blotting, anti-fish IgH-1 antiserum detected the IgMs of all fish species except banded houndshark. Anti-fish IgH-2 antiserum clearly reacted with the IgMs of only three of the fish species (seabream, yellowtail and rainbow trout). Attempts to use the antisera to measure fish antibody titer by ELISA were unsuccessful. These results demonstrate that anti-fish IgH-1 peptide polyclonal antiserum is a potentially applicable tool for detecting immunoglobulins in various fish species by Western blotting. - 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

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

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