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- Table of Contents
15 Q&As
Facts about Breakpoint cluster region protein.
GTPase-activating protein for RAC1 and CDC42.
Promotes the exchange of RAC or CDC42-bound GDP by GTP, thereby activating them.Displays serine/threonine kinase activity. .
Human | |
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Gene Name: | BCR |
Uniprot: | P11274 |
Entrez: | 613 |
Belongs to: |
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No superfamily |
ALL; ALLD22S11; BCR; BCR1; breakpoint cluster region protein; breakpoint cluster region; CMLEC 2.7.11.1; D22S662; PHL; PHLFLJ16453; Renal carcinoma antigen NY-REN-26
Mass (kDA):
142.819 kDA
Human | |
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Location: | 22q11.23 |
Sequence: | 22; NC_000022.11 (23180509..23318037) |
Cell junction, synapse, postsynaptic density. Cell projection, dendritic spine. Cell projection, axon. Cell junction, synapse.
If you require an antibody that can identify IgG-switched B cells or a brand new antibody to recognize the Boster Bio Anti-IL2RA antibody, it is crucial to be aware of the specificity and affinity of the antibodies. Boster validates antibodies in multiple platforms by using positive and negative samples to ensure that the antibodies are highly specific and have high affinity. Boster gives product credits to early reviewers. It doesn't matter if you're a young stage scientist or an experienced veteran, you are able to benefit from Boster's knowledge and experience.
Boster Bio Anti-IL2RA Antibodies are taken from Human IL-2Ralpha. The antibody is part of the Picoband(tm) catalog. This antibody reacts with Human, Mouse, and Rat IL-2R alpha. Each species has its own antigenic sequence , and the antibodies are tested in accordance with Boster's strict protocols.
The BCR marker can be used to determine the fate of plasma cells as well as other B cells within the body. Memory B cells are the main type of B cells, that have various functions, and their fate is determined by the BCR that is expressed on their surface. They are also known as memory B cells, and their fate is determined by their BCR affinity and isotype. This feature provides memory B cells with flexibility, which is essential for their effective response to an antigen.
The BCR marker, a molecule found within blood cells has been used for over 100 years to assess the immune response to infection. It is also utilized in the treatment of cancer and other infectious diseases. It can also be utilized to test antiviral medications. There are many ways to test for this marker. A few of the most commonly used uses of this marker are described in the following paragraphs.
The immune system is largely affected by the variations in B cell fates, which are GC-dependent or antigen-dependent. While B cells that have GC-dependent fates are capable of controlling the initial infection, long-lived memory B cells can also be created. The GC reaction, which can take several days, allows GC B cells to differentiate into long-lived blood cells and memory B cells, respectively.
After being activated by antigen B cells that are naive move into secondary lymphoid organs and undergo differentiation. These B cells are able to interact with antigen-specific preactivated cells T cells, that trigger a response. The antigen-activated cells stimulate proliferation and differentiation into germinal-centre B cells, which eventually differentiate into short-lived plasma cells.
Self-renewing memory cells On the other hand grow slowly and respond quickly to exposure. They develop into plasma cells and germinal centresand undergo another round affinity maturation. They produce the same antigens when they differentiate back to memory cells. This results in an increased response to subsequent challenges to antigens. Plasma cells produce anti-inflammatory antibodies that protect the living.
A study of memory B cells found that people with a small amount of memory B cells do have high levels of antigen-specific antibodies. The titer of vaccinia-specific antibodies did not correlate with the number of memory B cells. This is thought to indicate that memory B cells may have two independent arms. The presence of plasma with a long lifespan cells is necessary for one arm, whereas the other is dependent on existence and function of B memory cells. The removal of memory cells by itself did not affect the levels of preexisting antibody.
However, the fate of B cells is not easy to determine. Low affinity antigens may not necessarily exclude GC cells from the phase 1. In fact, they could enter GCs and then differentiate into memory or high affinity plasma cells. Phase 1 differentiation doesn't require low affinity antigens. In fact these cells can be used to control GC-independent cell differentiation.
During the process of editing receptors B cells that have VH4-34, VH4-409, and VH4-59 genes display a distal Jk bias and a large proportion of they bind to their cognate IgG-receptor molecules. This bias towards the distal is related to B cell selection and is a major factor in the process receptor editing.
These experiments show that the CdCS lineage is highly specialized and has a very specific antigenic reactivity and a unique set of V genes. They also show a striking selection of hallmarks of autoimmunity, including evidence of receptor editing. They may be a result of the mechanism of tolerization, which causes their differentiation and is a factor in class-related selection. Cd-CS could also be a tolerization mechanism as this lineage includes both naturally-occurring B cells and mutational autospecific ones.
We identified VH4-34-using cells within three CdCS populations using only one mAb. These B cells were enhanced in the PC population and GC population. Analyses of statistical data did not reveal any statistically significant differences between the two B cell populations, but the VH4-34-utilizing population accounted for more than 20 percent of CdCS B cells in two donors.
In contrast, plasma cells undergo terminal differentiation, a process governed by a gene-regulatory network and environmental stimuli. These cells can be transformed into plasma cells with a short lifespan or memory cells that can last for a long time. Plasmablasts are transient populations of B cells that serve as precursors of plasma cells or effector cells that are terminally differentiated during an ongoing immune response. These cells secrete large amounts of antibodies.
The signalling pathways of Boster Bio are governed by genes that regulate various aspects of cell survival. The hypoxia signaling pathway is characterized by the oxygen environment being depleted. Hypoxia stimulates the proliferation of cancerous cells. HIF activity regulates the expression of genes that are involved in angiogenesis, metastasis and survival. HIF and other molecules within the pathway are potential therapeutic targets. They also regulate several pathways, including Jak-Stat3, NF-kB , and PI3K/Akt/mTOR.
The maintenance of the BCR population is dependent on the CD40 signalling pathway. Changes in CD40 could affect the ability B-cells to switch between Ig classes. This can lead to abnormal antibody production. It is also associated with inflammation-related autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. You can download the free Boster Bio signalling pathway software to study the function of CD40 in the maintenance of B cell fate.
Hedgehog signaling is another important pathway. This pathway is vital for the proper differentiation of embryonic cells. Different mammals have three Hedgehog homologues. The Sonic hedgehog is the best examined during vertebrate limb formation. Hedgehog signaling also regulates adult stem cells that are vital for maintaining and growing organs. Therefore, problems with Hedgehog signaling can lead to tumor development and birth defects.
The activity of mTOR is controlled by the AKT/TSC1–TSC2 signaling pathway. TSC2 inhibits the small GTPase Rheb, that is necessary to activate the mTORC1. TSC2 inhibits Rheb's phosphorylation AMPK. Thus, a large amount of HIF is important for heart protection and ensuring the longevity of heart muscle cells.
PMID: 3285291 by Lifshitz B., et al. bcr genes and transcripts.
PMID: 7665185 by Chissoe S.L., et al. Sequence and analysis of the human ABL gene, the BCR gene, and regions involved in the Philadelphia chromosomal translocation.