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BLNK encodes a cytoplasmic linker or adaptor protein that plays a critical role in B cell development. Zusätzlich bieten wir Ihnen B-Cell Linker Antikörper (212) und B-Cell Linker Proteine (13) und viele weitere Produktgruppen zu diesem Protein an.
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The pre-B-cell receptor (pre-BCR (zeige BCR ELISA Kits)) signaling molecules BLNK, BTK (zeige BTK ELISA Kits) and BANK1 (zeige BANK1 ELISA Kits) were positively regulated by the ZFP521 gene, leading to enhancement of the pre-BCR (zeige BCR ELISA Kits) signaling pathway.
Authors demonstrate leukemogenicity of PAX5 (zeige PAX5 ELISA Kits)-PML (zeige PML ELISA Kits) by introducing it into normal mouse pro-B cells; B-cell linker protein (Blnk) is repressed by PAX5 (zeige PAX5 ELISA Kits)-PML (zeige PML ELISA Kits) in leukemia cells; enforced expression of Blnk increases survival despite introduction of PAX5 (zeige PAX5 ELISA Kits)-PML (zeige PML ELISA Kits).
B-cell linker protein expression contributes to controlling allergic and autoimmune diseases by mediating IL-10 (zeige IL10 ELISA Kits) production in regulatory B cells.
Tumor suppressor BLNK is a target of transcriptional activation by PU.1 and Spi-B (zeige SPIB ELISA Kits) in the B cell lineage.
a novel negative feedback regulation of BCR (zeige BCR ELISA Kits) signaling by HPK1-mediated phosphorylation, ubiquitination, and subsequent degradation of the activated BLNK
CMTM7 (zeige 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 (zeige SH3KBP1 ELISA Kits) are both required for the onset and progression phases of B-cell antigen receptor signal transduction.
malignant transformation of Btk (zeige BTK ELISA Kits)/Slp65 double-deficient pre-B cells is independent of deregulated V(D)J recombination activity.
Swip-1 (zeige WSB1 ELISA Kits) provides a membrane scaffold that is required for the Syk (zeige SYK ELISA Kits)-, SLP-65-, and PLCgamma2 (zeige PLCG2 ELISA Kits)-dependent BCR (zeige 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 (zeige BCR ELISA Kits) activation.
early Ca(2 (zeige CA2 ELISA Kits)+) fluxing provides feed-forward signal amplification by promoting anchoring of the PLCgamma2 (zeige PLCG2 ELISA Kits) C2 domain to phospho-SLP65.
up-regulation of BLNK is associated with RUNX1 (zeige RUNX1 ELISA Kits) mutations in cytogenetically normal acute myeloid leukemia (zeige 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 (zeige SYK ELISA Kits) is required to link phosphorylated SLP-65 to Ca(2 (zeige CA2 ELISA Kits)+) mobilization.
Plasmacytoid dendritic cells express a signalosome consisting of Lyn (zeige LYN ELISA Kits), Syk (zeige SYK ELISA Kits), Btk (zeige BTK ELISA Kits), Slp65 (Blnk) and PLCgamma2 (zeige PLCG2 ELISA Kits). Triggering CD303 leads to tyrosine phosphorylation of Syk (zeige SYK ELISA Kits), Slp65, PLCgamma2 (zeige 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