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Yasuyuki Ohkawa

Researcher at Kyushu University

Publications -  216
Citations -  7699

Yasuyuki Ohkawa is an academic researcher from Kyushu University. The author has contributed to research in topics: Chromatin & Gene. The author has an hindex of 40, co-authored 200 publications receiving 5981 citations. Previous affiliations of Yasuyuki Ohkawa include University of Massachusetts Medical School & Osaka City University.

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Interleukin-10-Producing Plasmablasts Exert Regulatory Function in Autoimmune Inflammation

TL;DR: It is found that plasmablasts in the draining lymph nodes (dLNs), but not splenic B lineage cells, predominantly expressed IL-10 during experimental autoimmune encephalomyelitis (EAE), and IRF4 positively regulated IL- 10 production that can inhibit dendritic cell functions to generate pathogenic T cells.
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Chromatin remodelling in mammalian differentiation: lessons from ATP-dependent remodellers.

TL;DR: A role for ATP-dependent remodelling in regulating the balance between proliferation and differentiation is revealed, and intriguing links between chromatin remodelling and other cellular processes during differentiation, including recombination, genome organization and the cell cycle are uncovered.
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Interaction of reactive astrocytes with type I collagen induces astrocytic scar formation through the integrin–N-cadherin pathway after spinal cord injury

TL;DR: In a mouse model of spinal cord injury, pharmacological blockade of reactive astrocyte–type I collagen interaction preventedAstrocytic scar formation, thereby leading to improved axonal regrowth and better functional outcomes, and reveal environmental cues regulating astROcytic fate decisions, thereby providing a potential therapeutic target for CNS injury.
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MyoD Targets Chromatin Remodeling Complexes to the Myogenin Locus Prior to Forming a Stable DNA-Bound Complex

TL;DR: It is observed that the homeodomain factor Pbx1, which cooperates with MyoD to stimulate myogenin expression, is constitutively bound to theMyoD promoter in a SWI/SNF-independent manner, suggesting a two-step mechanism in which Myo D initially interacts indirectly with the myogenIn promoter and attracts chromatin-remodeling enzymes, which then facilitate direct binding by MyOD and other regulatory proteins.
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CHD8 haploinsufficiency results in autistic-like phenotypes in mice

TL;DR: It is shown that mice heterozygous for Chd8 mutations manifest ASD-like behavioural characteristics including increased anxiety, repetitive behaviour, and altered social behaviour, consistent with the notion that CHD8 haploinsufficiency is a highly penetrant risk factor for ASD.