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Facts about Integrin alpha-IIb.
It recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain. Following activation integrin alpha- IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen.
Human | |
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Gene Name: | ITGA2B |
Uniprot: | P08514 |
Entrez: | 3674 |
Belongs to: |
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integrin alpha chain family |
CD41 antigen; CD41; CD41BHPA3; GP2B; GP2Bintegrin alpha-IIb; GPalpha IIb; GPIIb; GTA; HPA3; Integrin alpha 2b; integrin, alpha 2b (platelet glycoprotein IIb of IIb/IIIa complex, antigenCD41); integrin, alpha 2b (platelet glycoprotein IIb of IIb/IIIa complex, antigenCD41B); ITGA2b; ITGAB; platelet fibrinogen receptor, alpha subunit; Platelet membrane glycoprotein IIb; platelet-specific antigen BAK
Mass (kDA):
113.377 kDA
Human | |
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Location: | 17q21.31 |
Sequence: | 17; NC_000017.11 (44372181..44389649, complement) |
Isoform 1 and isoform 2 are expressed in platelets and megakaryocytes, but not in reticulocytes. Not detected in Jurkat, nor in U937 cell lines (PubMed:2351656). Isoform 3 is expressed in prostate adenocarcinoma, as well as in several erythroleukemia, prostate adenocarcinoma and melanoma cell lines, including PC-3, DU-145, HEL, WM983A, WM983B and WM35. Not detected in platelets, nor in normal prostate (at protein level) (PubMed:9809974).
Membrane; Single-pass type I membrane protein.
If you're looking for high-affinity primary antibodies deubiquitinase USP15 or high-affinity primary antibodies, you're in the right place. There are a variety of resources to help you answer your questions and optimize your experiments to get better results. Additionally every researcher is faced with an issue with their experiment at some point or another. While most mistakes can be eliminated by proper controls, they still happen. Troubleshooting guides can be a useful aid to identify and eliminate common causes of error.
High-affinity antibody are antibodies that have high affinity for antigens. They are produced by the immune system by a process called affinity maturation. B cells produce antibodies through affinity maturation in the course of the primary response. It isn't known the process by which memory B-cells develop. There are many methods to generate high-affinity antibodies. These include cell lineage analysis, molecular biology and Clonal Sequencing.
High-affinity primary antibodies consist of single molecules of IgG with varying molecular weights. They connect to a single epitope with high affinity but have a lower specificity. Monoclonal antibodies need to be applied in a concentrated manner, and washing methods should not alter the binding. High-affinity primary antibodies can be made through clone-selection, but they are not as prevalent.
AFCs with high affinity were detected in bone marrow after 14 days after the immunization. Antigen-specific AFCs had high affinity and only a few VH gene mutations. The cells with mutations had higher Trp to Leu ratios around position 33. Hence, high-affinity primary antibodies are more efficient and cost-effective when it comes to the production of vaccines. Scientists can improve diagnosis using the research of these researchers, they believe.
Our understanding of the immune system's ability to recognize and respond has been improved by studying the evolutionary roots of high-affinity primary antibodies. Next-generation sequencing (NGS), which increases sample depth has revolutionized the process of antibody repertoire analysis. It has allowed researchers to determine the L and H chains of the individual immune cells, which provides the genetic record for the evolution of processes. In addition to genomics research, new discoveries have been discovered through crystal structures of affinity-matured antibodies.
The affinity-matured antibody was initially studied as a protein antigen, not an hapten. Different stages of affinity maturation were utilized to characterize the antibody responses to Hapten. In addition, to the number of somatic mutations, the increase in affinity was not due to an increase in hydrogen bonds or salt bridges or an increase in the buried surface area. The higher affinity was due to the burial a hydrophobic layer and an improvement in the shape complementarity of the VH-HEL interface.
The GC B-cell population undergoes affinity maturation, which is reflected in the amount of IgG1 in serum. In the course of immunization in the primary phase it was possible to collect serum samples from a group of mice on a regular basis and tested for total IgG1 titre and high-affinity NP-binding IgG1 amount. The first samples collected on day seven showed high affinity NP-specific IgG1, which increased steadily until the 21st day.
A new study has demonstrated that antibody CH58 was isolated from an individual who participated in the RV144 HIV vaccine effectiveness trial. It targets Lys169 in HIV V2 peptide and is highly mutational. The structure of the germ-line precursor of CH58 has been determined in both bound and unliganded V2 peptide. The ligand bound conformation is driven by the formation of two salt bridges in affinity maturity.
USP15 regulates the polyubiquitylation of Neosubstrates. It is able to deubiquitylate GS (a protein which is polyubiquitylated, both in vivo and in vitro). It is also able to deubiquitylate GS with other polymers, like phospholipids. Further research is required to discover the molecular mechanism by which USP15 can deubiquitylate the proteins it targets.
USP15 blocks CRBN in cancer cells. This enzyme is a substrate for CRL4CRBN which is an E3 Ubiquitin Ligase, and is an immediate target for thalidomide teratology. This enzyme is downstream of CRL4CRBN, and upstream from the proteasome. Since USP15 is essential for the degrading of target proteins it may help improve the clinical outcomes of patients with MM. The USP15 protein could also be a biomarker for response to IMiD therapy.
Three distinct UbVs also attached to the catalyticdomain, and locked the active site into a closed conformation. Additionally, one UbV linked to two DUSP domains, creating an unusual dimer that is strand-swapped. With the availability of inhibitors further studies on the role of USP15 is possible.
Additionally, the inhibitors of USP15 hindered hypertrophic scar fibroblast growth and migration. However, USP15 overexpression showed an opposite trend. It promoted the proliferation of hypertrophic scar tissue by increasing their migration, invasion, collagen deposition, and , consequently, increased the number of them. These results suggest that USP15 may be an interesting target for the treatment of hypertrophic scar.
CB5083 or PR-619 inhibited USP15 and PR-619, which also blocked the interaction between USP15 (glutamine-stimulated) cells and GS. These inhibitors function in a similar way to the endogenous USP15 that interacts directly and directly with GS. It hinders the growth and development of GBM cells by lowering USP15 levels.
USP15 can also be linked to altered signaling in a variety of cell types. The overexpression of USP15 increased the levels of several proteins including TbRI and Smad. It also increased COL1 and a-SMA. It was also linked to a significant decrease in NFkB signaling. USP15 is a key player in signaling across a variety of cell types.
PMID: 2439501 by Poncz M., et al. Structure of the platelet membrane glycoprotein IIb. Homology to the alpha subunits of the vitronectin and fibronectin membrane receptors.
PMID: 2345548 by Frachet P., et al. GPIIb and GPIIIa amino acid sequences deduced from human megakaryocyte cDNAs.
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