BLNK
Reactivity: Human
WB, ELISA, IHC
Host: Rabbit
Polyclonal
unconjugated
Sample Volume
20 μL
Restrictions
For Research Use only
Format
Liquid
Buffer
Aqueous buffered solution containing BSA and ≤0.09 % sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
4 °C
Storage Comment
Store undiluted at 4°C and protected from prolonged exposure to light. Do not freeze. The antibody was conjugated with R-PE under optimum conditions, and unconjugated antibody and free PE were removed.
Espeli, Mancini, Breton, Poirier, Schiff: "Impaired B-cell development at the pre-BII-cell stage in galectin-1-deficient mice due to inefficient pre-BII/stromal cell interactions." in: Blood, Vol. 113, Issue 23, pp. 5878-86, (2009) (PubMed).
B cell activation is initiated by crosslinking the B cell receptor, which leads to activation of non-receptor protein tyrosine kinases (PTK), including Btk, Syk, and three Src kinases, Fyn, Lyn, and Blk. Activated PTKs then phosphorylate multiple cellular proteins involved in B lymphocyte signaling. Syk is responsible for the tyrosine phosphorylation of B cell linker protein (BLNK), a member of the SLP-76 family of adapter proteins. Phosphorylation of human BLNK at tyrosines 84, 178, and 189 (Y84, Y178, and Y189) creates docking sites for PLCg2, leading to the activation of downstream signaling pathways. The J117-1278 monoclonal antibody recognizes the phosphorylated Y84 of BLNK.