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BLNK encodes a cytoplasmic linker or adaptor protein that plays a critical role in B cell development. De plus, nous expédions B-Cell Linker Anticorps (212) et B-Cell Linker Protéines (13) et beaucoup plus de produits pour cette protéine.
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The pre-B-cell receptor (pre-BCR (Montrer BCR Kits ELISA)) signaling molecules BLNK, BTK (Montrer BTK Kits ELISA) and BANK1 were positively regulated by the ZFP521 gene, leading to enhancement of the pre-BCR (Montrer BCR Kits ELISA) signaling pathway.
Authors demonstrate leukemogenicity of PAX5 (Montrer PAX5 Kits ELISA)-PML (Montrer PML Kits ELISA) by introducing it into normal mouse pro-B cells; B-cell linker protein (Blnk) is repressed by PAX5 (Montrer PAX5 Kits ELISA)-PML (Montrer PML Kits ELISA) in leukemia cells; enforced expression of Blnk increases survival despite introduction of PAX5 (Montrer PAX5 Kits ELISA)-PML (Montrer PML Kits ELISA).
B-cell linker protein expression contributes to controlling allergic and autoimmune diseases by mediating IL-10 (Montrer IL10 Kits ELISA) production in regulatory B cells.
Tumor suppressor BLNK is a target of transcriptional activation by PU.1 and Spi-B in the B cell lineage.
a novel negative feedback regulation of BCR (Montrer BCR Kits ELISA) signaling by HPK1-mediated phosphorylation, ubiquitination, and subsequent degradation of the activated BLNK
CMTM7 (Montrer CMTM7 Kits ELISA) functions to link sIgM and BLNK in the plasma membrane.
Live cell imaging and co-immunoprecipitation experiments confirmed that both SLP65 and CIN85 are both required for the onset and progression phases of B-cell antigen receptor signal transduction.
malignant transformation of Btk (Montrer BTK Kits ELISA)/Slp65 double-deficient pre-B cells is independent of deregulated V(D)J recombination activity.
Swip-1 provides a membrane scaffold that is required for the Syk (Montrer SYK Kits ELISA)-, SLP-65-, and PLCgamma2 (Montrer PLCG2 Kits ELISA)-dependent BCR (Montrer BCR Kits ELISA)-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 (Montrer BCR Kits ELISA) activation.
early Ca(2 (Montrer CA2 Kits ELISA)+) fluxing provides feed-forward signal amplification by promoting anchoring of the PLCgamma2 (Montrer PLCG2 Kits ELISA) C2 domain to phospho-SLP65.
up-regulation of BLNK is associated with RUNX1 (Montrer RUNX1 Kits ELISA) mutations in cytogenetically normal acute myeloid leukemia (Montrer BCL11A Kits ELISA).
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 (Montrer SYK Kits ELISA) is required to link phosphorylated SLP-65 to Ca(2 (Montrer CA2 Kits ELISA)+) mobilization.
Plasmacytoid dendritic cells express a signalosome consisting of Lyn (Montrer LYN Kits ELISA), Syk (Montrer SYK Kits ELISA), Btk (Montrer BTK Kits ELISA), Slp65 (Blnk) and PLCgamma2 (Montrer PLCG2 Kits ELISA). Triggering CD303 leads to tyrosine phosphorylation of Syk (Montrer SYK Kits ELISA), Slp65, PLCgamma2 (Montrer PLCG2 Kits ELISA) & 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