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1.
FIGURE 3.

FIGURE 3. From: Tumor Suppressor Ras Association Domain Family 5 (RASSF5/NORE1) Mediates Death Receptor Ligand-induced Apoptosis.

Reduced activation of the stress-activated p38 and JNK kinases in RASSF5 depleted cells treated with TNF-α. U2OS cells transfected with control (Cont.) or RASSF5 siRNA and treated with 25 ng/ml TNF-α and cycloheximide for the indicated times were analyzed by Western blotting with phospho-p38, p38, phospho-JNK, JNK phospho-p42/p44, p42/p44, and β-actin antibodies. Letter p in circle, phospho.

Jikyoung Park, et al. J Biol Chem. 2010 November 5;285(45):35029-35038.
2.
FIGURE 2.

FIGURE 2. From: Tumor Suppressor Ras Association Domain Family 5 (RASSF5/NORE1) Mediates Death Receptor Ligand-induced Apoptosis.

RASSF5 interacts with MST1 and other components of Hippo signaling pathway. A, U2OS cells cotransfected with FLAG-RASSF5 and either MST1, WW45, LATS1, or YAP1 were immunoprecipitated (IP) with either FLAG, MST1, WW45, LATS1, or YAP1 antibodies and analyzed by Western blotting (WB). B, 4-week-old mouse brain lysates were immunoprecipitated with anti-RASSF5, anti-MST1, or anti-YAP1 antibody and analyzed by immunoblotting. C, U2OS cells were transfected with control or MST1, WW45, LATS1, or YAP1 siRNA and treated with varying concentrations of TNF-α along with cycloheximide. Cell survival was measured as described.

Jikyoung Park, et al. J Biol Chem. 2010 November 5;285(45):35029-35038.
3.
FIGURE 7.

FIGURE 7. From: Tumor Suppressor Ras Association Domain Family 5 (RASSF5/NORE1) Mediates Death Receptor Ligand-induced Apoptosis.

Rassf5-deficient MEFs are predisposed to K-RasG12V-induced transformation. A, soft agar assay. Immortalized Rassf5+/+ and Rassf5−/− MEFs stably expressing empty vector or K-RasG12V were grown in soft agar for 21 days, and the colonies were counted. The experiment was performed in triplicate and repeated three times using two independently derived MEFs. B, representative images taken under phase-contrast microscope of immortalized Rassf5+/+ and Rassf5−/− MEFs stably expressing K-RasG12V are shown. C, immortalized Rassf5+/+ and Rassf5−/− MEFs stably expressing empty vector or K-RasG12V were injected subcutaneously into nude mice, and the animals were sacrificed at 3–5 weeks after injection. The tumors were dissected and weighed.

Jikyoung Park, et al. J Biol Chem. 2010 November 5;285(45):35029-35038.
4.
FIGURE 4.

FIGURE 4. From: Tumor Suppressor Ras Association Domain Family 5 (RASSF5/NORE1) Mediates Death Receptor Ligand-induced Apoptosis.

Inactivation of Rassf5 by gene targeting. A, a scheme of Rassf5 targeting strategy. Homologous recombination will delete exons 3–5 and insert the neomycin gene. The triangles indicate LoxP sequences. B, Southern blot analysis of HindIII-digested mouse ES genomic DNA. Wild type (5.6-kb) and targeted (13.8-kb) alleles are indicated. C, PCR analysis of tail DNA. Wild type (177 bp) and targeted (228 bp) bands are indicated. D, mouse brain lysates from 4-week-old Rassf5 wild type and mutant animals or Rassf5+/+ and Rassf5−/− MEFs were analyzed by immunoblotting with anti-RASSF5 antibody. Anti-β-actin was used for loading control. KO, knock-out.

Jikyoung Park, et al. J Biol Chem. 2010 November 5;285(45):35029-35038.
5.
FIGURE 5.

FIGURE 5. From: Tumor Suppressor Ras Association Domain Family 5 (RASSF5/NORE1) Mediates Death Receptor Ligand-induced Apoptosis.

Rassf5-deficient MEFs are resistant to TNF-α- and TRAIL-induced apoptosis. A, wild type and Rassf5-null MEFs were treated with varying concentrations of TNF-α and cycloheximide, and cell survival was measured as described. B, wild type and Rassf5-null MEFs treated with 25 ng/ml TNF-α and cycloheximide for the indicated times were analyzed by Western blotting with PARP and β-actin antibodies. The arrow indicates cleaved PARP. C, Rassf5+/+ and Rassf5−/− MEFs were treated with varying concentrations of TRAIL (Peprotech) and cycloheximide (10 μg/ml) for 18 h, and cells stained for annexin V and propidium iodide (PI) were analyzed by FACSCalibur (BD Biosciences). The number in each quadrant indicates percentage of cells positive for annexin V, PI or both. Quadrant I, early apoptosis population (with annexin V, without PI); quadrant II, late apoptosis population (with annexin V and PI); quadrant III, necrosis population (without annexin V, with PI). CON, control.

Jikyoung Park, et al. J Biol Chem. 2010 November 5;285(45):35029-35038.
6.
FIGURE 1.

FIGURE 1. From: Tumor Suppressor Ras Association Domain Family 5 (RASSF5/NORE1) Mediates Death Receptor Ligand-induced Apoptosis.

RASSF5 depletion results in reduced TNF-α-mediated apoptosis. A, U2OS cells were transfected with control or RASSF5 siRNA and treated with varying concentrations of TNF-α along with 10 μg/ml cycloheximide. Cell survival was measured with Cell Counting Kit-8 (Dojindo). B, U2OS cells transfected with control or RASSF5 siRNA and treated with 25 ng/ml TNF-α and 10 μg/ml cycloheximide for indicated times were analyzed by Western blotting using PARP, Pro-CASP3, and Pro-CASP8 antibodies. An arrow indicates cleaved PARP. C, U2OS cells transfected with control or RASSF5 siRNA and treated with 25 ng/ml TNF-α and 10 μg/ml cycloheximide for 4 h were fixed, immunostained with anti-BAX antibody, and analyzed by fluorescence microscopy. The percentage of BAX-positive cells/total cells from four or five randomly chosen fields was calculated from three independent experiments, and the representative images are shown.

Jikyoung Park, et al. J Biol Chem. 2010 November 5;285(45):35029-35038.
7.
FIGURE 6.

FIGURE 6. From: Tumor Suppressor Ras Association Domain Family 5 (RASSF5/NORE1) Mediates Death Receptor Ligand-induced Apoptosis.

Rassf5-deficient mice are resistant to TNF-α-induced apoptosis. A, Rassf5 wild type (n = 7) and mutant mice (n = 4) were injected via tail vein with d-galactosamine and TNF-α. The time of death was recorded for each mouse. B, Rassf5 wild type and mutant mice were injected with TNF-α as in A, and all of the animals were sacrificed at 6 h before death (n = 3 for each genotype). Paraffin-embedded sections of liver were analyzed by H & E and TUNEL staining. Control liver (Rassf5+/−) from an uninjected animal is shown. C, positive TUNEL-stained cells (from B) were counted from at least seven randomly chosen fields, and the average number of TUNEL-positive cells/field is shown (n = 3 for each genotype). D, liver extracts from Rassf5 wild type and mutant TNF-α-treated animals (n = 3 for each genotype) were analyzed by Western blotting with Pro-CASP3, MST1, phospho-H2B, H2B, and α-tubulin antibodies. H&E, hematoxylin and eosin.

Jikyoung Park, et al. J Biol Chem. 2010 November 5;285(45):35029-35038.

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