Results: 5

1.
Figure 4

Figure 4. From: BCR and its mutants, the reciprocal t(9;22)-associated ABL/BCR fusion proteins, differentially regulate the cytoskeleton and cell motility.

Migration of hematopoietic progenitor 32D cells expressing t(9;22) translocation products into M2-10B4 spheroids. A. Expression of the transgenes in 32D cells was controlled by Western blot analysis using α-ABL and α-BCR antibodies as indicated. B. Percentage of 32D cells expressing the indicated transgenes that migrated into the spheroids. The bar graphs represent the averages of triplicates with standard deviation. One representative experiment out of three performed is given.

Xiaomin Zheng, et al. BMC Cancer. 2006;6:262-262.
2.
Figure 3

Figure 3. From: BCR and its mutants, the reciprocal t(9;22)-associated ABL/BCR fusion proteins, differentially regulate the cytoskeleton and cell motility.

Rho-like small GTPase activation in Rat-1 cells expressing t(9;22) translocation products. A. Expression of the transgenes in Rat-1 cells was controlled by Western blot analysis using α-ABL and α-BCR antibodies as indicated. B. The indicated activated small GTPase was pulled down and revealed by the specific antibody. Rac*, cdc42*, Rho* – activated forms; total Rac, cdc42, Rho – total amount revealed in the cell lysates used for the pull down. One representative experiment of three performed is given.

Xiaomin Zheng, et al. BMC Cancer. 2006;6:262-262.
3.
Figure 1

Figure 1. From: BCR and its mutants, the reciprocal t(9;22)-associated ABL/BCR fusion proteins, differentially regulate the cytoskeleton and cell motility.

Modular organization of the main t(9;22) translocation products. The protein sizes are not to scale. CC – coiled coil oligomerization interface; S/T kinase – serine/threonine kinase domain; DH – dbl homology domain; PH – pleckstrin homology domain; GAP – GTPase activation domain; STEV – PDZ-binding motif; SH3, SH2 – Src-homology domain 3 and 2; Y-kinase – tyrosine kinase domain (SH1), AB – actin-binding domain; der 9 and der 22 – derivative 9 and 22.

Xiaomin Zheng, et al. BMC Cancer. 2006;6:262-262.
4.
Figure 5

Figure 5. From: BCR and its mutants, the reciprocal t(9;22)-associated ABL/BCR fusion proteins, differentially regulate the cytoskeleton and cell motility.

Adhesion on endothelium and endothelial transmigration of hematopoietic progenitor 32D cells expressing t(9;22) translocation products. A. Percentage of 32D cells that were adherent to HUVEC in the absence/presence (-/+) of TNFα under different shear stresses (0.1 and 2 dyn/cm2) in a flow chamber. The bar graphs represent the averages of three fields counted with standard deviation. One representative experiment out of three performed is given. B. Percentage of 32D cells that migrated through a HUVEC layer in a transwell assay. The bar graphs represent the average of triplicates with standard deviation. One representative experiment out of three performed is given.

Xiaomin Zheng, et al. BMC Cancer. 2006;6:262-262.
5.
Figure 2

Figure 2. From: BCR and its mutants, the reciprocal t(9;22)-associated ABL/BCR fusion proteins, differentially regulate the cytoskeleton and cell motility.

Cytoskeleton modeling in Rat-1 cells expressing t(9;22) translocation products. A. The provirus used for transduction of the cell line. Expression of the transgenes is driven by the 5'-LTR (long-term repeat), whereas the EGFP-reporter gene is under the control of the CMV promoter (CMV-P). B. Provirus used for the expression of the transgenes. The sizes are not to scale. C. Expression of the transgenes in Rat-1 cells was controlled by Western blot analysis using α-ABL and α-BCR antibodies as indicated. D. Rat-1 cells expressing the indicated transgenes stained with phalloidin to reveal the actin cytoskeleton. mock – empty vector infected cells as control. Control – mock infected Rat-1 cells; Rac* – V12Rac (constitutively activated form of Rac), cdc42* – V12cdc42 (constitutively activated form of cdc42), Rho* – V14Rho (constitutively activated form of Rho). The bottom panel shows the Rat-1 cells co-expressing BCR/ABL together with BCR or its mutants.

Xiaomin Zheng, et al. BMC Cancer. 2006;6:262-262.

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