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BLNK encodes a cytoplasmic linker or adaptor protein that plays a critical role in B cell development. Additionally we are shipping B-Cell Linker Antibodies (212) and B-Cell Linker Proteins (13) and many more products for this protein.
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The pre-B-cell receptor (pre-BCR (show BCR ELISA Kits)) signaling molecules BLNK, BTK (show BTK ELISA Kits) and BANK1 (show BANK1 ELISA Kits) were positively regulated by the ZFP521 gene, leading to enhancement of the pre-BCR (show BCR ELISA Kits) signaling pathway.
Authors demonstrate leukemogenicity of PAX5 (show PAX5 ELISA Kits)-PML (show PML ELISA Kits) by introducing it into normal mouse pro-B cells; B-cell linker protein (Blnk) is repressed by PAX5 (show PAX5 ELISA Kits)-PML (show PML ELISA Kits) in leukemia cells; enforced expression of Blnk increases survival despite introduction of PAX5 (show PAX5 ELISA Kits)-PML (show PML ELISA Kits).
B-cell linker protein expression contributes to controlling allergic and autoimmune diseases by mediating IL-10 (show IL10 ELISA Kits) production in regulatory B cells.
Tumor suppressor BLNK is a target of transcriptional activation by PU.1 and Spi-B (show SPIB ELISA Kits) in the B cell lineage.
a novel negative feedback regulation of BCR (show BCR ELISA Kits) signaling by HPK1-mediated phosphorylation, ubiquitination, and subsequent degradation of the activated BLNK
CMTM7 (show CMTM7 ELISA Kits) functions to link sIgM and BLNK in the plasma membrane.
Live cell imaging and co-immunoprecipitation experiments confirmed that both SLP65 and CIN85 (show SH3KBP1 ELISA Kits) are both required for the onset and progression phases of B-cell antigen receptor signal transduction.
malignant transformation of Btk (show BTK ELISA Kits)/Slp65 double-deficient pre-B cells is independent of deregulated V(D)J recombination activity.
Swip-1 (show WSB1 ELISA Kits) provides a membrane scaffold that is required for the Syk (show SYK ELISA Kits)-, SLP-65-, and PLCgamma2 (show PLCG2 ELISA Kits)-dependent BCR (show BCR ELISA Kits)-induced calcium flux.
malignant transformation of Slp65(-/-) pre-B cells involves disruption of the p19(Arf)-Mdm2-p53 tumor suppressor pathway
vesicular signaling scaffolds are required for B cell activation indicates that vesicles may deliver preassembled signaling cargo to sites of BCR (show BCR ELISA Kits) activation.
early Ca(2 (show CA2 ELISA Kits)+) fluxing provides feed-forward signal amplification by promoting anchoring of the PLCgamma2 (show PLCG2 ELISA Kits) C2 domain to phospho-SLP65.
up-regulation of BLNK is associated with RUNX1 (show RUNX1 ELISA Kits) mutations in cytogenetically normal acute myeloid leukemia (show BCL11A ELISA Kits).
16 of the 34 childhood pre-B acute lymphoblastic leukaemia samples that were tested showed a complete loss or drastic reduction of SLP-65 expression
The BLNK protein is present in the majority of mediastinal B cell lymphomas.
In B cells SLP-65 exists in a 180 kDa complex as well as in monomeric form.
V(H) gene rearrangement represents a frequent feature in B-lymphoid malignancy, which can be attributed to SLP65 deficiency in many cases.
Syk (show SYK ELISA Kits) is required to link phosphorylated SLP-65 to Ca(2 (show CA2 ELISA Kits)+) mobilization.
Plasmacytoid dendritic cells express a signalosome consisting of Lyn (show LYN ELISA Kits), Syk (show SYK ELISA Kits), Btk (show BTK ELISA Kits), Slp65 (Blnk) and PLCgamma2 (show PLCG2 ELISA Kits). Triggering CD303 leads to tyrosine phosphorylation of Syk (show SYK ELISA Kits), Slp65, PLCgamma2 (show PLCG2 ELISA Kits) & cytoskeletal proteins.
This gene encodes a cytoplasmic linker or adaptor protein that plays a critical role in B cell development. This protein bridges B cell receptor-associated kinase activation with downstream signaling pathways, thereby affecting various biological functions. The phosphorylation of five tyrosine residues is necessary for this protein to nucleate distinct signaling effectors following B cell receptor activation. Mutations in this gene cause hypoglobulinemia and absent B cells, a disease in which the pro- to pre-B-cell transition is developmentally blocked. Deficiency in this protein has also been shown in some cases of pre-B acute lymphoblastic leukemia. Alternatively spliced transcript variants have been found for this gene.
, B-cell linker protein
, b-cell linker protein-like
, B-cell adapter containing a SH2 domain protein
, B-cell adapter containing a Src homology 2 domain protein
, cytoplasmic adapter protein
, lymphocyte antigen 57
, src homology 2 domain-containing leukocyte protein of 65 kDa
, B cell adaptor containing SH2 domain
, B cell linker protein
, B-cell activation
, Src homology 2 domain-containing leukocyte protein of 65 kDa
, Src homology [SH2] domain-containing leukocyte protein of 65 kD
, B cell linker protein BLNK
, B-cell adapter SH2 domain-containing protein