B-Cell Linker (BLNK) ELISA Kits

Mouse (Murine) B-Cell Linker (BLNK) Interaktionspartner

1. The pre-B-cell receptor (pre-BCR) signaling molecules BLNK, BTK and BANK1 were positively regulated by the ZFP521 gene, leading to enhancement of the pre-BCR signaling pathway.

2. Authors demonstrate leukemogenicity of PAX5-PML by introducing it into normal mouse pro-B cells; B-cell linker protein (Blnk) is repressed by PAX5-PML in leukemia cells; enforced expression of Blnk increases survival despite introduction of PAX5-PML.

3. B-cell linker protein expression contributes to controlling allergic and autoimmune diseases by mediating IL-10 production in regulatory B cells.

4. Tumor suppressor BLNK is a target of transcriptional activation by PU.1 and Spi-B in the B cell lineage.

5. a novel negative feedback regulation of BCR signaling by HPK1-mediated phosphorylation, ubiquitination, and subsequent degradation of the activated BLNK

6. CMTM7 functions to link sIgM and BLNK in the plasma membrane.

7. 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.

8. malignant transformation of Btk/Slp65 double-deficient pre-B cells is independent of deregulated V(D)J recombination activity.

9. Swip-1 provides a membrane scaffold that is required for the Syk-, SLP-65-, and PLCgamma2-dependent BCR-induced calcium flux.

10. malignant transformation of Slp65(-/-) pre-B cells involves disruption of the p19(Arf)-Mdm2-p53 tumor suppressor pathway

11. role in B cell Ag receptor-mediated antigen processing

12. The direct recruitment of BLNK to immunoglobulin alpha couples the B-cell antigen receptor to distal signaling pathways

13. role for BLNK and perhaps BCR signaling, in the regulation of kappa light chain expression and continued immature B cell differentiation

14. BLNK as a direct target of the transcription factor Pax5

15. SLP-65 regulates a developmental program that promotes differentiation and limits pre-B cell expansion, thereby acting as a tumor suppressor.

16. Differentiation regulator SLP-65 (an adaptor protein also called BLNK or BASH) inhibits pre-B-cell leukaemia in mice

17. constitutive active Btk can substitute for SLP-65 as a tumor suppressor.

18. adaptor proteins LAT and SLP-76 are involved in pre-BCR signaling, thereby rescuing arrested murine SLP-65(-/-) pre-B cells

19. SLP65/BLNK is a substrate of SHP-1.

20. bone marrow-derived macrophages mice lacking both SLP-76 and SLP-65 demonstrated normal FcgammaR-mediated activation

Human B-Cell Linker (BLNK) Interaktionspartner

1. vesicular signaling scaffolds are required for B cell activation indicates that vesicles may deliver preassembled signaling cargo to sites of BCR activation.

2. early Ca(2+) fluxing provides feed-forward signal amplification by promoting anchoring of the PLCgamma2 C2 domain to phospho-SLP65.

3. up-regulation of BLNK is associated with RUNX1 mutations in cytogenetically normal acute myeloid leukemia.

4. 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.

5. 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

6. The BLNK protein is present in the majority of mediastinal B cell lymphomas.

7. In B cells SLP-65 exists in a 180 kDa complex as well as in monomeric form.

8. V(H) gene rearrangement represents a frequent feature in B-lymphoid malignancy, which can be attributed to SLP65 deficiency in many cases.

9. Syk is required to link phosphorylated SLP-65 to Ca(2+) mobilization.

10. Plasmacytoid dendritic cells express a signalosome consisting of Lyn, Syk, Btk, Slp65 (Blnk) and PLCgamma2. Triggering CD303 leads to tyrosine phosphorylation of Syk, Slp65, PLCgamma2 & cytoskeletal proteins.

11. BLNK prevents aneuploidy by inhibiting cytokinesis.

12. BLNK recruits active H-Ras to the BCR complex, which is essential for sustained surface expression of BCR in the form of the cap and for the signal leading to functional ERK activation

13. Data show that SLP-65 phosphorylation acts upstream for signal initiation and also downstream during selective processing of the B cell receptor signal.

14. Identifies BLNK as a potential target for the protein-tyrosine phosphatase SHP-1.