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Results: 8

1.
FIG. 6.

FIG. 6. From: Myosin VI Is a Mediator of the p53-Dependent Cell Survival Pathway.

Nuclear localization of myosin VI is increased by p53. Whole-cell extracts (WCE) or nuclear extracts (NE) were prepared from H1299 cells uninduced or induced to express p53. The level of myosin VI, cis-Golgi marker GM130, p53, and actin was quantified by Western blot analysis.

Eun Joo Jung, et al. Mol Cell Biol. 2006 March;26(6):2175-2186.
2.
FIG. 5.

FIG. 5. From: Myosin VI Is a Mediator of the p53-Dependent Cell Survival Pathway.

(A and B) Intracellular localization of myosin VI is altered in RKO cells by DNA damage in a p53-dependent manner. Parental RKO and RKO-p53-KD cells were mock treated or treated with doxorubicin (DOX). These cells were then stained with anti-p53, anti-myosin VI, and DAPI. (C) Colocalization of myosin VI with trans-Golgi marker TGN p230. Parental RKO cells were mock treated or treated with nutlin or camptothecin (CPT).

Eun Joo Jung, et al. Mol Cell Biol. 2006 March;26(6):2175-2186.
3.
FIG. 1.

FIG. 1. From: Myosin VI Is a Mediator of the p53-Dependent Cell Survival Pathway.

Myosin VI is a novel target gene of p53. (A) Myosin VI is induced by p53 in a time-dependent manner. (B) Induction of myosin VI by wild-type and various mutated forms of p53. (C) Myosin VI is induced by DNA damage in a p53-dependent manner. RKO and LS174T were either untreated (−) or treated (+) with 300 nM camptothecin for 24 h. Northern blots were probed with 32P-labeled cDNA for myosin VI, p21, and/or GAPDH.

Eun Joo Jung, et al. Mol Cell Biol. 2006 March;26(6):2175-2186.
4.
FIG. 2.

FIG. 2. From: Myosin VI Is a Mediator of the p53-Dependent Cell Survival Pathway.

Level of myosin VI, but not GBF, GM130 and p115, is increased by DNA damage in a p53-dependent manner. (A) The induction of myosin VI by DNA damage is dependent on p53. RKO and RKO-p53-KD were untreated (−) or treated with dimethyl sulfoxide (DMSO), 0.2 μg/ml of doxorubicin (DOX), or 200 nM camptothecin (CPT). (B) The level of myosin VI protein is increased by DNA damage in a time-dependent manner. RKO cells were untreated (−) or treated with 0.2 μg/ml of DMSO, 0.2 μg/ml of doxorubicin, or 100 nM camptothecin for 12, 24, and 48 h. (C) The level of myosin VI, but not other Golgi proteins, is increased by DNA damage in a p53-dependent manner. RKO, LS174T, and HeLa cells were treated with 0, 0.1, 0.3, or 0.5 μg/ml of doxorubicin. Whole-cell extracts were analyzed by Western blotting with antibodies as indicated. Actin was analyzed as a loading control.

Eun Joo Jung, et al. Mol Cell Biol. 2006 March;26(6):2175-2186.
5.
FIG. 8.

FIG. 8. From: Myosin VI Is a Mediator of the p53-Dependent Cell Survival Pathway.

Myosin VI knockdown accelerates DNA damage-induced apoptosis. (A) Myo6-KD-87 cells were uninduced (control), induced to express siRNA against myosin VI (myosin VI-KD), treated with 1.0 μg/ml of DOX (DOX), or induced to express siRNA against myosin VI and treated with 1.0 μg/ml of doxorubicin (DOX + Myosin VI-KD). DNA histogram analysis was performed as described in Materials and Methods. The percentage of sub-G1 (M1) cells represents apoptotic cells, whereas M2, M3, and M4 represent cells in G0-G1, S, and G2-M, respectively. (B) DNA damage-induced apoptotic response is enhanced by myosin VI knockdown. Both Myo6-KD-87 and Myo6-KD-3 cells, which were uninduced or induced to express siRNA against myosin VI, were untreated or treated with 1.0 μg per ml of doxorubicin. The expression level of myosin VI, p53, p21, PARP, caspase 8, and actin was quantified by Western blot analysis. (C) Knockdown of myosin VI leads to impaired phosphorylation of p53 via ATM and increased expression of Fas, a target of p53. The experiment was performed as in panel B.

Eun Joo Jung, et al. Mol Cell Biol. 2006 March;26(6):2175-2186.
6.
FIG.4.

FIG.4. From: Myosin VI Is a Mediator of the p53-Dependent Cell Survival Pathway.

Intracellular localization of myosin VI is altered by wild-type p53, but not mutant p53 or wild-type p73β. (A) Myosin VI is induced by wild-type (wt) p53, but not mutant (mut) p53(R273H). H24-208 cells were uninduced (control), induced to express wild-type p53, induced to express mutant p53(R273H), or induced to express both for 48 h. The expression level of wild-type p53, mutant p53, myosin VI, p21, and GBF was quantified by Western blot analysis. Actin was analyzed as a loading control. (B) Myosin VI is induced by wild-type p53, but not wild-type p73β. H24-112 cells were uninduced (control), induced to express wild-type p73β, induced to express wild-type p53, or induced to express both for 48 h. The expression level of p73β, p53, myosin VI, p21, and p115 was quantified by Western blot analysis. (C) The intracellular localization of myosin VI is altered by wild-type p53, which is inhibited by mutant p53(R273H). Immunofluorescence staining was performed as described in Materials and Methods. p53 was stained green, whereas myosin VI was stained red. Nuclei were stained blue. con, control. (D) The intracellular localization of myosin VI is altered by wild-type p53, but not wild-type p73β. (E) Colocalization of myosin VI with trans-Golgi marker TGN p230. (F) Cell cycle arrest is not sufficient to alter cellular localization of myosin VI. H1299 cells were uninduced or induced to express p53, p73β, or both. The cell cycle profile was determined by DNA histogram analysis 36 h following induction of p53, p73, or both.

Eun Joo Jung, et al. Mol Cell Biol. 2006 March;26(6):2175-2186.
7.
FIG. 3.

FIG. 3. From: Myosin VI Is a Mediator of the p53-Dependent Cell Survival Pathway.

Myosin VI is a direct target of the p53 transcription factor. (A) Schematic presentation of the human myosin VI gene locus and luciferase (Luc) reporter constructs. Box A represents a potential p53-binding site from nt −347 to −325, whereas box B is a GC-rich region from nt −171 to −72. (B) The GC-rich region in the myosin VI promoter is responsive to wild-type (wt) p53, but not mutant (mut) p53. The luciferase assay was performed as described in Materials and Methods. con, control. (C) Schematic presentation of 11 additional myosin VI promoter/reporter constructs with deletion in the GC-rich region. (D and E) The GC-rich region is required for p53 transactivation of the myosin VI promoter. (F and G) Schematic representation of the myosin VI and p21 promoters with the locations of the transcription start site, p53-responsive elements, and primers used for ChIP assays. (H) p53 binds directly to the myosin VI promoter. The ChIP assay was performed as described in Materials and Methods. (I) Wild-type p53, but not mutant p53(R249S), binds directly to the myosin VI promoter. α-p53 and α-419, anti-p53 and anti-419 antibodies, respectively.

Eun Joo Jung, et al. Mol Cell Biol. 2006 March;26(6):2175-2186.
8.
FIG. 7.

FIG. 7. From: Myosin VI Is a Mediator of the p53-Dependent Cell Survival Pathway.

Myosin VI knockdown attenuates the activation of p53 and impairs myosin VI-mediated maintenance of Golgi complex integrity. (A) Myosin VI is required for efficient stabilization of p53 by DNA damage. Myo6-KD-87, in which myosin VI is inducibly knocked down by siRNA, was uninduced (−) or induced (+) to express siRNA against myosin VI for 3 days followed by treatment with 0 or 5 μg/ml of doxorubicin for 0.5, 2, or 4 h. The expression level of myosin VI, p53, and γ-H2AX was quantified by Western blot analysis. Actin was analyzed as an internal loading control. (B) Intracellular localization of p53 and myosin VI in Myo6-KD-87 RKO cells. RKO cells were uninduced (top panel), treated with 1.0 μg/ml of doxorubicin (DOX) for 16 h (second panel), induced to express siRNA against myosin VI (third panel), or induced to express siRNA against myosin VI and treated with 1.0 μg/ml of doxorubicin (bottom panel). Immunofluorescence staining was performed as described in Materials and Methods. p53 was stained green, whereas myosin VI was stained red. Nuclei were stained blue. (C) Intracellular localization of myosin VI and Golgi marker protein TGN p230 in Myo6-KD-87 RKO cells. The experiments were performed similarly to those in panel B. TGN p230 was stained green, whereas myosin VI was stained red. Nuclei were stained blue.

Eun Joo Jung, et al. Mol Cell Biol. 2006 March;26(6):2175-2186.

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