Showing papers by "Aydin Tozeren published in 2013"
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26 Mar 2013
TL;DR: In this paper, the human body structure, including Muscles, tendons, ligaments, and bones, is described, as well as the internal forces and internal forces of the Musculoskeletal system.
Abstract: Human Body Structure: Muscles, Tendons, Ligaments, and Bones.- Laws of Motion: Snowflakes, Airborne Balls, Pendulums.- Particles in Motion: Method of Lumped Masses and Jumping, Sit-Ups, Push-Ups.- Bodies in Planar Motion: Jumping, Diving, Push-Ups, Back Curls.- Statics: Tug-of-War, Weight Lifting, Trusses, Cables, Beams.- Internal Forces and the Human Body: Complexity of the Musculoskeletal System.- Impulse and Momentum: Impulsive Forces and Crash Mechanics.- Energy Transfers: In Pole Vaulting, Running, and Abdominal Workout.- Three-Dimensional Motion: Somersaults, Throwing, and Hitting Motions.
119 citations
TL;DR: It is concluded that cyclin D1 induction of Dicer coordinates microRNA biogenesis, which significantly correlates in luminal A and basal-like subtypes of human breast cancer.
Abstract: Cyclin D1 encodes the regulatory subunit of a holoenzyme that phosphorylates the pRB protein and promotes G1/S cell-cycle progression and oncogenesis. Dicer is a central regulator of miRNA maturation, encoding an enzyme that cleaves double-stranded RNA or stem-loop-stem RNA into 20-25 nucleotide long small RNA, governing sequence-specific gene silencing and heterochromatin methylation. The mechanism by which the cell cycle directly controls the non-coding genome is poorly understood. Here we show that cyclin D1(-/-) cells are defective in pre-miRNA processing which is restored by cyclin D1a rescue. Cyclin D1 induces Dicer expression in vitro and in vivo. Dicer is transcriptionally targeted by cyclin D1, via a cdk-independent mechanism. Cyclin D1 and Dicer expression significantly correlates in luminal A and basal-like subtypes of human breast cancer. Cyclin D1 and Dicer maintain heterochromatic histone modification (Tri-m-H3K9). Cyclin D1-mediated cellular proliferation and migration is Dicer-dependent. We conclude that cyclin D1 induction of Dicer coordinates microRNA biogenesis.
60 citations
TL;DR: DACH1 binds p53 to inhibit NSCLC cellular growth, contributing to the inhibition of colony formation and cell-cycle arrest.
Abstract: Hyperactive EGF receptor (EGFR) and mutant p53 are common genetic abnormalities driving the progression of non-small cell lung cancer (NSCLC), the leading cause of cancer deaths in the world. The Drosophila gene Dachshund (Dac) was originally cloned as an inhibitor of hyperactive EGFR alleles. Given the importance of EGFR signaling in lung cancer etiology, we examined the role of DACH1 expression in lung cancer development. DACH1 protein and mRNA expression was reduced in human NSCLC. Reexpression of DACH1 reduced NSCLC colony formation and tumor growth in vivo via p53. Endogenous DACH1 colocalized with p53 in a nuclear, extranucleolar location, and shared occupancy of -15% of p53-bound genes in ChIP sequencing. The C-terminus of DACH1 was necessary for direct p53 binding, contributing to the inhibition of colony formation and cell-cycle arrest. Expression of the stem cell factor SOX2 was repressed by DACH1, and SOX2 expression was inversely correlated with DACH1 in NSCLC. We conclude that DACH1 binds p53 to inhibit NSCLC cellular growth.
53 citations