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- Table of Contents
Facts about B-cell linker protein.
Modulates AP1 activation. Significant for the activation of NF-kappa-B and NFAT.
Mouse | |
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Gene Name: | Blnk |
Uniprot: | Q9QUN3 |
Entrez: | 17060 |
Belongs to: |
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No superfamily |
AGM4; B cell linker protein; BASH; B-cell adapter containing a SH2 domain protein; B-cell adapter containing a Src homology 2 domain protein; B-cell linker protein; B-cell linker; BLNK; BLNK-s; Cytoplasmic adapter protein; Ly57; MGC111051; SLP65; SLP-65BLNK-S; SLP65Ly57; Src homology 2 domain-containing leukocyte protein of 65 kDa
Mass (kDA):
50.671 kDA
Mouse | |
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Location: | 19 C3|19 34.26 cM |
Sequence: | 19; |
Expressed in the spleen and weakly in thymus, no expression was seen in liver, testis, or brain. Expressed in B- cell lines representing different developmental stages from the pre-B to the plasma cell stage, but not in a T-cell or a fibroblast cell line.
This article will discuss the history, uses, and origins the BLNK mark. We will also be discussing the history of Boster, and the incubation. Continue reading to learn more. The BLNK marker will help you save time and improve your research, no matter if you're a student, researcher or healthcare professional.
Steven Boster's fascinating history is fascinating. Boster, who is often called "he that converts science to the lavatory," was a pioneer in IHC technology, and has created hundreds of primary antibodies. PicoKine(tm), Boster's patented ELISA platform made it possible for him to become the largest China-based antibody catalog by late 1990s. Boster is also the inventor on proprietary trade secrets that allow laboratories around the globe to order high-sensitivity ELISA Kits.
Boster's book can be divided into three sections. Each section is dedicated to a different aspect about slavery in the American South. Boster opens the book by telling the story about Tom Wilson, a disabled slave who was featured prominently in abolitionist propaganda. Boster shows how the story of Tom Wilson is tied to the exhibition of slaves for prospective buyers. This story illustrates the difference between slaves, fugitives.
BLNK-/ B cells show defective proliferation in response to anti-IgM and LPS stimulation. This phenomenon was examined by stimulating wild-type B cell cultures for 48 hours with increasing amounts of goat anti-mouse IgM (ab)2 fragment. A MTT colorimetric analyze was used to quantify cell proliferation. The experiment was conducted using B cells from different age groups.
Anti-IgM BLNK-/ B cell proliferation is halted by BrdUrd incompatibility. This allows us to differentiate between B cells within different cell cycles. BrdUrd will be found in cells that are in the S phase. BrdUrd will not be found in cells that are in the G0/G1 phase.
BLNK is a transcription factor that interacts with tyrosine-phosphorylated targets. By recruiting these targets to the BCR complex, the BCR is activated. These proteins can be activated by BLNK. The gene encoding BLNK is found in several tissues. BLNK expression in the B cell line DT40 is reduced.
BLNK/B cells undergo apoptosis faster than wild-type cells. BLNK-/ cells exhibit significantly reduced DNA content when cultured overnight on a medium containing or without goat anti-mouse IgMF(ab)’2 fragment. PI staining revealed a decrease in size and forward scatter profiles. BLNK/B cells are more sensitive to LPS-induced death than wild-type cells.
BLNK-/ B cells exhibit defective NF-kB activity. This is due in part to the inability of cRel or p50 to induce degradation inhibitory kB proteins. These BLNK/ B cells resemble xid B cell lines with mutations in Bruton’s tyrosine kinase. BLNK-/ cells not only affect NF-kB activation but also display defective T-cell-independent immune responses.
Interestingly, when BLNK-/ B cells were treated with anti-IgM antibodies, degradation of IkBa and p50 of NF-kB was impaired. These results suggest that NF-kB may not be able to translocate to its nucleus due to impaired degradation of IkB proteins. These results show that BLNK is required to activate NF-kB in the presence anti-IgM antibodies.
B cells are activated through the role of BLNK. It is essential for the activation of transcription factors and tyrosine-kinases by BCR. BLNK is also critical in the pre-BCR dependent progression of B cell survival, development, and proliferation as well as in T independent immune responses. This protein is also known by the names SLP-65 and BASH.
The rd_CopyMarkers commands will copy markers to other layers in order for you to use them in compositions. The rd_MapTextFileToMarkers command sets the keyframes of the text layer using the text file in the corresponding layers. The rd_MarkerNavigatorcommand creates a panel allowing the user to view markers. Finally, rd_RemoveMarkers will clear all markers from the selected layer.
Gene 1 & 2 in the TCGA dataset show similar performance, even though they come from different types. These genes were not co-expressed in immune and brain tumors. This may be due to tumor-intrinsic transcription of these genes. Additionally, the blood-brain border limits the dynamic range immune cell abundance in cancerous tumors. This marker is useful for developing treatment strategies if you are a cancer researcher.
PMID: 9697839 by Fu C., et al. BLNK: a central linker protein in B cell activation.
PMID: 9705962 by Wienands J., et al. SLP-65: a new signaling component in B lymphocytes which requires expression of the antigen receptor for phosphorylation.