CRK Primary Antibody
|Formulation||Ascitic fluid containing 0.03% sodium azide.|
|Immunogen||Purified recombinant fragment of human CRK expressed in E. Coli. |
|Shipping Information||This product will ship in a box containing blue ice at a temperature of 4°C. Learn More|
|ICC (Immunocytochemistry)||1/200 - 1/1000|
|IHC_P(Immunohistochemistry)||1/200 - 1/1000|
|FCM (Flow Cytometry)||1/200 - 1/400|
|WB (Western Blot)||1/500 - 1/2000|
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Figure 1: Western blot analysis using CRK mAb against human CRK (AA: 1-204) recombinant protein. (Expected MW is 48.4 kDa)
Figure 2: Western blot analysis using CRK mAb against HEK293 (1) and CRK(AA: 1-204)-hIgGFc transfected HEK293 (2) cell lysate.
Figure 3: Immunohistochemical analysis of paraffin-embedded rectum cancer tissues using CRK mouse mAb with DAB staining.
Figure 4: Immunohistochemical analysis of paraffin-embedded bladder cancer tissues using CRK mouse mAb with DAB staining.
Figure 5: Immunofluorescence analysis of 3T3-L1 cells using CRK mouse mAb (green). Blue: DRAQ5 fluorescent DNA dye. Red: Actin filaments have been labeled with Alexa Fluor-555 phalloidin.
Figure 6: Flow cytometric analysis of MCF-7 cells using CRK mouse mAb (blue) and negative control (red).
Red: Control Antigen (100ng); Purple: Antigen (10ng); Green: Antigen (50ng); Blue: Antigen (100ng);
This gene encodes a member of an adapter protein family that binds to several tyrosine-phosphorylated proteins. The product of this gene has several SH2 and SH3 domains (src-homology domains) and is involved in several signaling pathways, recruiting cytoplasmic proteins in the vicinity of tyrosine kinase through SH2-phosphotyrosine interaction. The N-terminal SH2 domain of this protein functions as a positive regulator of transformation whereas the C-terminal SH3 domain functions as a negative regulator of transformation. Two alternative transcripts encoding different isoforms with distinct biological activity have been described.
|References (references)||1. Seikagaku. 2009 May;81(5):361-76. |
2. Mol Cancer Res. 2009 Sep;7(9):1582-92.