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B cell linker

BLNK, SLP-65, BASH, B cell linker protein
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 encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: BCR, Syk, Btk, Src, CAN
Papers using BLNK antibodies
Phospholipase C-γ2 couples Bruton's tyrosine kinase to the NF-κB signaling pathway in B lymphocytes
Kitamura Daisuke et al., In The Journal of Experimental Medicine, 2000
... was used for immunoprecipitation, while goat Ab (anti-BLNK, C-19, Santa Cruz Biotechnology, Inc.) was used for ...
Papers on BLNK
BLNK is a selective target of repression by PAX5-PML in the differentiation block that leads to the development of acute lymphoblastic leukemia.
Kiyoi et al., Nagoya, Japan. In J Biol Chem, Jan 2016
Among the transactivation targets of PAX5, BLNK was selectively repressed in leukemia cells and enforced BLNK expression abrogated differentiation block induced by PAX5-PML, indicating the importance of BLNK repression for the differentiation block.
Quantitative expression of regulatory and differentiation-related genes in the key steps of human hematopoiesis: The LeukoStage Database.
Hrušák et al., Praha, Czech Republic. In Differentiation, Jan 2016
Expression levels of regulatory molecules (such as the IKZF, GATA, HOX, FOX, NOTCH and CEBP families, as well as SPI-1/PU1 and PAX5) and lineage-specific molecules (including CD2, CD14, CD79A, and BLNK) may be compared between pathological and physiological cells.
ZFP521 contributes to pre-B-cell lymphomagenesis through modulation of the pre-B-cell receptor signaling pathway.
Tsuruyama et al., Kyoto, Japan. In Oncogene, Dec 2015
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.
[Genetic basis of immune response of lymphocyte-like cells in the mucosal immune system of Lampetra japonica].
Qingwei et al., Dalian, China. In Yi Chuan, Nov 2015
The results of real-time fluorescence quantitative PCR showed that the expression levels of Lck, Fyn and Zap70 were up-regulated after immune stimulation while those of Syk, Btk and Blnk were not changed significantly, indicating the activation of TCR-like signal transduction pathway after antigen stimulation in lamprey gill tissues.
Concomitant high expression of Toll-like receptor (TLR) and B-cell receptor (BCR) signalling molecules has clinical implications in mantle cell lymphoma.
Mansoor et al., Calgary, Canada. In Hematol Oncol, Oct 2015
Higher levels of BTK/SYK/BLNK/CARD11/PLCG signalosome and lower expression of MALT1/BCL10 genes suggested tonic pattern of BCR activation.
B-cell receptor signalling and its crosstalk with other pathways in normal and malignant cells.
Mraz et al., Brno, Czech Republic. In Eur J Haematol, Mar 2015
In lymphoma B cells, the balance of initiation, amplitude and duration of BCR activation can be influenced by a specific immunoglobulin structure, the expression and mutations of adaptor molecules (like GAB1, BLNK, GRB2, CARD11), the activity of kinases (like LYN, SYK, PI3K) or phosphatases (like SHIP-1, SHP-1 and PTEN) and levels of microRNAs.
Homonuclear decoupling for enhancing resolution and sensitivity in NOE and RDC measurements of peptides and proteins.
Bax et al., Bethesda, United States. In J Magn Reson, 2014
Application of band-selective homonuclear (BASH) (1)H decoupling pulses during acquisition of the (1)H free induction decay is shown to be an efficient procedure for removal of scalar and residual dipolar couplings between amide and aliphatic protons.
FOXO1 transcription factor: a critical effector of the PI3K-AKT axis in B-cell development.
Juszczyński et al., Warsaw, Poland. In Int Rev Immunol, 2014
FOXO1 deficiency impairs B-cell development, due to decreased expression of its critical target genes, that include early B-cell factor (EBF1), IL-7 receptor, recombination activating genes (RAG1 and 2), activation-induced cytidine deaminase (AID), L-selectin, and BLNK.
Systems biology of primary CNS lymphoma: from genetic aberrations to modeling in mice.
Siebert et al., Köln, Germany. In Acta Neuropathol, 2014
Several important pathways, i.e., the B cell receptor (BCR), the toll-like receptor, and the nuclear factor-κB pathway, are activated frequently due to genetic changes affecting genes like CD79B, SHIP, CBL, BLNK, CARD11, MALT1, BCL2, and MYD88.
RUNX1 mutations are associated with poor outcome in younger and older patients with cytogenetically normal acute myeloid leukemia and with distinct gene and MicroRNA expression signatures.
Bloomfield et al., Columbus, United States. In J Clin Oncol, 2012
Because RUNX1 mutations were more common in older patients and almost never coexisted with NPM1 mutations, RUNX1 mutation-associated expression signatures were derived in older, NPM1 wild-type patients and featured upregulation of genes normally expressed in primitive hematopoietic cells and B-cell progenitors, including DNTT, BAALC, BLNK, CD109, RBPMS, and FLT3, and downregulation of promoters of myelopoiesis, including CEBPA and miR-223.
Down-regulation of B cell receptor signaling by hematopoietic progenitor kinase 1 (HPK1)-mediated phosphorylation and ubiquitination of activated B cell linker protein (BLNK).
Tan et al., Houston, United States. In J Biol Chem, 2012
a novel negative feedback regulation of BCR signaling by HPK1-mediated phosphorylation, ubiquitination, and subsequent degradation of the activated BLNK
A self-reinforcing regulatory network triggered by limiting IL-7 activates pre-BCR signaling and differentiation.
Singh et al., Chicago, United States. In Nat Immunol, 2012
Attenuation of IL-7 signaling resulted in upregulation of the transcription factors Foxo1 and Pax5, which coactivated many pre-B cell genes, including Rag1, Rag2 and Blnk.
Identification of CMTM7 as a transmembrane linker of BLNK and the B-cell receptor.
Kitamura et al., Noda, Japan. In Plos One, 2011
CMTM7 functions to link sIgM and BLNK in the plasma membrane.
The B-cell antigen receptor signals through a preformed transducer module of SLP65 and CIN85.
Wienands et al., Göttingen, Germany. In Embo J, 2011
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.
Pre-B-cell leukemias in Btk/Slp65-deficient mice arise independently of ongoing V(D)J recombination activity.
Hendriks et al., Rotterdam, Netherlands. In Leukemia, 2011
malignant transformation of Btk/Slp65 double-deficient pre-B cells is independent of deregulated V(D)J recombination activity.
Swiprosin-1/EFhd2 controls B cell receptor signaling through the assembly of the B cell receptor, Syk, and phospholipase C gamma2 in membrane rafts.
Mielenz et al., Erlangen, Germany. In J Immunol, 2010
Swip-1 provides a membrane scaffold that is required for the Syk-, SLP-65-, and PLCgamma2-dependent BCR-induced calcium flux.
[Osteoimmunology: an integrated vision of immune and bone systems].
Jurdic et al., Lyon, France. In Med Sci (paris), 2009
A recent study from H. Takayanagi's group has shown that the tyrosine kinases Btk and Tec form a multiprotein complex with adaptor molecules such as BLNK, that is able to integrate these two signaling pathways and thus stimulate osteoclastogenesis.
Primary B cell immunodeficiencies: comparisons and contrasts.
Campana et al., Memphis, United States. In Annu Rev Immunol, 2008
Mutations in Btk, components of the pre-B cell and B cell receptor (lambda5, Igalpha, Igbeta), or the scaffold protein BLNK account for approximately 90% of patients with defects in early B cell development.
SLP-65 regulates immunoglobulin light chain gene recombination through the PI(3)K-PKB-Foxo pathway.
Jumaa et al., Freiburg, Germany. In Nat Immunol, 2008
Although the essential role of the adaptor protein SLP-65 in pre-B cell differentiation is established, the molecular mechanism underlying its function is poorly understood.
Tyrosine kinases Btk and Tec regulate osteoclast differentiation by linking RANK and ITAM signals.
Takayanagi et al., Sendai, Japan. In Cell, 2008
RANK and ITAM signaling results in formation of a Btk(Tec)/BLNK(SLP-76)-containing complex and PLCgamma-mediated activation of an essential calcium signal.
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