Figure 4
Figure 4. LCP1 is integral to the CXCL12-driven migration of leukemic cells. (A) Immunoblot analysis of MEC1 or 697 cell lines stably transduced with either an empty vector construct or a shRNA lentiviral knockdown vector to confirm absence of LCP1. GAPDH was used as a loading control. (B) Transwell migration analysis of MEC1 empty vector and MEC1-LCP1 knockdown (KD) in the presence of the chemokine CXCL12 to evaluate chemotactic importance of LCP1. (C) Transwell migration analysis of 697-empty vector and 697-LCP1 knockdown in the presence of chemokine CXCL12 to evaluate importance of LCP1 to cellular chemotaxis. (B-C) Statistical analysis by two tailed Student t test; error bars represent standard error of the mean.

LCP1 is integral to the CXCL12-driven migration of leukemic cells. (A) Immunoblot analysis of MEC1 or 697 cell lines stably transduced with either an empty vector construct or a shRNA lentiviral knockdown vector to confirm absence of LCP1. GAPDH was used as a loading control. (B) Transwell migration analysis of MEC1 empty vector and MEC1-LCP1 knockdown (KD) in the presence of the chemokine CXCL12 to evaluate chemotactic importance of LCP1. (C) Transwell migration analysis of 697-empty vector and 697-LCP1 knockdown in the presence of chemokine CXCL12 to evaluate importance of LCP1 to cellular chemotaxis. (B-C) Statistical analysis by two tailed Student t test; error bars represent standard error of the mean.

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