100,944 research outputs found
The Science Enjoyed by Professor Alec T. Stewart
No full textLate Professor Stewart initiated and shaped the International Conference on Positron Annihilation (ICPA) series. As a first-generation experimental positron-annihilation scientist, he made full use of the angular correlation of annihilation radiation (ACAR) method. He applied this method to study Fermi surfaces of metals, positron wave-functions in crystals, positron-electron and -phonon many-body interactions, and the vacancy formation energy in solids. He also studied with this method positronium in liquids and solids (T. Hyodo, J. Phys. Conf. Series, 618 (2015) 012002). All these studies enjoyed by Professor Stewart will long be remembered by the positron study community.</jats:p
Improved constraints on chiral SU(3) dynamics from kaonic hydrogen
No full textAbstractA new improved study of K−–proton interactions near threshold is performed using coupled-channels dynamics based on the next-to-leading order chiral SU(3) meson–baryon effective Lagrangian. Accurate constraints are now provided by new high-precision kaonic hydrogen measurements. Together with threshold branching ratios and scattering data, these constraints permit an updated analysis of the complex K¯N and πΣ coupled-channels amplitudes and an improved determination of the K−p scattering length, including uncertainty estimates
Improved threshold constraints on coupled-channels chiral SU(3) dynamics from kaonic hydrogen
No full textTandem paired nicking promotes precise genome editing with scarce interference by p53. Hyodo et al.
No full textData and figures associated to a Cell Reports article "Tandem paired nicking promotes precise genome editing with scarce interference by p53" by Hyodo T et al
Tandem paired nicking promotes precise genome editing with scarce interference by p53. Hyodo et al.
No full textData and figures associated to a Cell Reports article "Tandem paired nicking promotes precise genome editing with scarce interference by p53" by Hyodo T et al
Tandem paired nicking promotes precise genome editing with scarce interference by p53. Hyodo et al.
No full textData and figures associated to a Cell Reports article "Tandem paired nicking promotes precise genome editing with scarce interference by p53" by Hyodo T et al
SATB1 and SATB2 play opposing roles in c-Myc expression and progression of colorectal cancer
No full textSpecial AT-rich sequence-binding protein 1 and 2 (SATB1/2) are nuclear matrix-associated proteins involved in chromatin remodeling and regulation of gene expression. SATB2 acts as a tumor suppressor in laryngeal squamous cell carcinoma and colon cancer, whereas SATB1 promotes the progression of numerous types of cancers. In this study, we examined the effects of SATB1 and SATB2 on the malignant characteristics of colorectal cancer cells. SATB1 and SATB2 expression were negatively correlated in colorectal cancer specimens. SATB1 expression was increased, whereas SATB2 expression was reduced, in colorectal cancer tissues compared to control tissues. Exogenous expression of SATB2 in colorectal cancer cells suppressed cell proliferation, colony formation and tumor proliferation in mice. c-Myc was reduced by SATB2 expression, and exogenous expression of c-Myc in SATB2-expressing cells restored proliferation, colony formation and in vivo tumor growth of colorectal cancer cells. We also showed that c-Myc reduction by SATB2 was mediated by the inactivation of ERK5. In contrast, SATB1 promoted c-Myc expression. The expression of SATB1 in colorectal cancer tissues was positively correlated with c-Myc expression, and SATB1 knockdown reduced c-Myc expression in colorectal cancer cells. Finally, we showed that SATB1 knockdown in colorectal cancer cells suppressed cell proliferation, colony formation and cell invasion. Our results reveal interesting features of how the structural homologs SATB1 and SATB2 exert opposing functions in colorectal tumorigenesis
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
SATB2 suppresses the progression of colorectal cancer cells via inactivation of MEK5/ERK5 signaling
No full textSpecial AT-rich sequence binding protein 2 (SATB2) is an evolutionarily conserved transcription factor that has multiple roles in neuronal development, osteoblast differentiation, and craniofacial patterning. SATB2 binds to the nuclear matrix attachment region, and regulates the expression of diverse sets of genes by altering chromatin structure. Recent studies have reported that high expression of SATB2 is associated with favorable prognosis in colorectal and laryngeal cancer; however, it remains uncertain whether SATB2 has tumor-suppressive functions in cancer cells. In this study, we examined the effects of SATB2 expression on the malignant characteristics of colorectal cancer cells. Expression of SATB2 repressed the proliferation of cancer cells in vitro and in vivo, and also suppressed their migration and invasion. Extracellular signal-regulated kinase 5 (ERK5) is a mitogen-activated protein kinase that is associated with an aggressive phenotype in various types of cancer. SATB2 expression reduced the activity of ERK5, and constitutive activation of ERK5 restored the proliferation, anchorage-independent growth, migration and invasion of SATB2-expressing cells. Our results demonstrate the existence of a novel regulatory mechanism of SATB2-mediated tumor suppression via ERK5 inactivation
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