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- 저자 : Hirofumi Kai (검색결과 6 건)
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( Kandai Nozu ),( Yutaka Takaoka ),( Hirofumi Kai ),( Minoru Takasato ),( Kensuke Yabuuchi ),( Tomohiko Yamamura ),( Tomoko Horinouchi ),( Nana Sakakibara ),( Takeshi Ninchoji ),( China Nagano ),( Kaz 대한신장학회 2020 Kidney Research and Clinical Practice Vol.39 No.4
Alport syndrome (AS) is a progressive inherited kidney disease characterized by hearing loss and ocular abnormalities. There are three forms of AS depending on inheritance mode: X-linked Alport syndrome (XLAS), autosomal recessive AS (ARAS), and autosomal dominant AS (ADAS). XLAS is caused by pathogenic variants in COL4A5, which encodes type IV collagen α5 chain, while ADAS and ARAS are caused by variants in COL4A3 or COL4A4, which encode type IV collagen α3 or α4 chain, respectively. In male XLAS or ARAS cases, end-stage kidney disease (ESKD) develops around a median age of 20 to 30 years old, while female XLAS or ADAS cases develop ESKD around a median age of 60 to 70 years old. The diagnosis of AS is dependent on either genetic or pathological findings. However, determining the pathogenicity of the variants detected by gene tests can be difficult. Recently, we applied the following molecular investigation tools to determine pathogenicity: 1) in silico and in vitro trimer formation assay of α345 chains to assess triple helix formation ability, 2) kidney organoids constructed from patients’ induced pluripotent stem cells to identify α5 chain expression on the glomerular basement membrane, and 3) in vitro splicing assay to detect aberrant splicing to determine the pathogenicity of variants. In this review article, we discuss the genetic background and novel assays for determining the pathogenicity of variants. We also discuss the current treatment approaches and introduce exon skipping therapy as one potential treatment option.
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Kumar, Narender,Harashima, Hirofumi,Kalve, Shweta,Bramsiepe, Jonathan,Wang, Kai,Sizani, Bulelani L.,Bertrand, Laura L.,Johnson, Matthew C.,Faulk, Christopher,Dale, Renee,Simmons, L. Alice,Churchman, M American Society of Plant Biologists 2015 The Plant cell Vol.27 No.11
<P>Although they play roles in many different developmental processes, the biochemical function of SMR-type CDK inhibitors is conserved among land plants.</P><P>The best-characterized members of the plant-specific SIAMESE-RELATED (SMR) family of cyclin-dependent kinase inhibitors regulate the transition from the mitotic cell cycle to endoreplication, also known as endoreduplication, an altered version of the cell cycle in which DNA is replicated without cell division. Some other family members are implicated in cell cycle responses to biotic and abiotic stresses. However, the functions of most SMRs remain unknown, and the specific cyclin-dependent kinase complexes inhibited by SMRs are unclear. Here, we demonstrate that a diverse group of SMRs, including an SMR from the bryophyte <I>Physcomitrella patens</I>, can complement an <I>Arabidopsis thaliana siamese</I> (<I>sim</I>) mutant and that both Arabidopsis SIM and <I>P. patens</I> SMR can inhibit CDK activity in vitro. Furthermore, we show that Arabidopsis SIM can bind to and inhibit both CDKA;1 and CDKB1;1. Finally, we show that <I>SMR2</I> acts to restrict cell proliferation during leaf growth in Arabidopsis and that <I>SIM</I>, <I>SMR1/LGO</I>, and <I>SMR2</I> play overlapping roles in controlling the transition from cell division to endoreplication during leaf development. These results indicate that differences in SMR function in plant growth and development are primarily due to differences in transcriptional and posttranscriptional regulation, rather than to differences in fundamental biochemical function.</P>
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The Role of Heat Shock Response in Insulin Resistance and Diabetes
Tatsuya Kondo,Hiroyuki Motoshima1,Motoyuki Igata,Junji Kawashima,Takeshi Matsumura,Hirofumi Kai,Eiichi Araki 대한당뇨병학회 2014 Diabetes and Metabolism Journal Vol.38 No.2
The expansion of life-style related diseases, such as metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM), appears to be unstoppable. It is also difficult to cease their complications in spite of many antidiabetic medications or intervention of public administration. We and our collaborators found that physical medicine using simultaneous stimulation of heat with mild electric current activates heat shock response, thereby reducing visceral adiposity, insulin resistance, chronic inflammation and improving glucose homeostasis in mice models of T2DM, as well as in humans with MS or T2DM. This combination therapy exerts novel action on insulin signaling, β-cell protection and body compositions, and may provide a new therapeutic alternative in diabetic treatment strategy.
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PM2.5로 자극한 폐상피세포의 $NF{\kappa}B$ 활성화에 NO의 역할
김경아,남혜윤,문제혁,정진숙,임영,Kim, Kyoung-Ah,Nam, Hae-Yun,Mun, Je-Hyeok,Jeong, Jin-Sook,Lim, Young,Kai, Hirofumi 대한결핵및호흡기학회 2002 Tuberculosis and Respiratory Diseases Vol.52 No.6
연구배경 : PM2.5는 호흡기질환의 악화 및 호흡기 질환에 의한 사망률과 밀접하게 관계가 있다. PM2.5에 의한 호흡기 염증반응의 악화가 그 원인으로 생각되나 염증반응의 조절기전은 확실하지 않다. 본연구에서는 PM2.5에 의한 폐장의 염증반응을 조절하는데 중요한 역할을 하는 전사인자인 $NF{\kappa}B$의 활성화 기전을 알아보아 염증 조절기전에 대한 이해를 높이고자 시도되었다. 방 법 : 폐상피세포주인 A549 세포에서 PM2.5 자극에 의한 $NF{\kappa}B$의 활성화 및 ROS, 그리고 RNS 분비를 관찰 하였다. iNOS 억제제인 L-NIL가 $NF{\kappa}B$ 활성화에 미치는 영향을 관찰하였다. 결 과 : PM2.5는 A549 세포에서 $NF{\kappa}B$의 활성화를 유도 하였다. PM2.5로 A549 세포를 자극시 즉각적인 RNS의 분비는 관찰되었으나 명확한 ROS의 증가는 관찰되지 않았다. RNS 억제제인 L-NIL 처리시 $NF{\kappa}B$ 활성화는 억제되었다. 결 론 : A549 세포에서 PM2.5에 의하여 유도된 즉각적인 $NF{\kappa}B$ 활성화 과정에는 RNS가 중요한 역할을 할 것으로 생각된다. Background : The present study was performed to further improve our understanding of molecular mechanisms involved in the activation of NFkB, a major transcriptional factor involved in the inflammatory response in the lung, by particulate matter in lung epithelial cells with an aerodynamic diameter of less than $2.5{\mu}m$(PM2.5). Materials and Methods : Immediate production of reactive oxygen species (ROS) and nitrogen species (RNS), with the PM2.5 induced expression of inducible nitric oxide synthase (iNOS), $I{\kappa}B$ degradation and $NF{\kappa}B$-dependent transcriptional activity, in 549 cells, were monitored. Addition, we also examined the effect of the iNOS inhibitor, L-N6-(1-iminoethyl) lysine hydrochloride (L-NIL), on the PM2.5-induced $NF{\kappa}B$ activation in A549 cells. Results : The rapid degradation of $I{\kappa}B$ and the increase of transcriptional activity of the $NF{\kappa}B$-dependent promotor were observed in A549 cells exposed to PM2.5. The immediate production of ROS in response to PM2.5 in A549 cells was not clearly detected, although immediate responses were observed in RAW264.7 cells. A 549 cells, cultured in the presence of PM2.5, produced an increase in NO, which was noticeably significant after 15 min of exposure with the expression of iNOS mRNA. The addition of L-NIL, an iNOS inhibitor, significantly inhibited the PM2.5-induced $I{\kappa}B$ degradation and the increase of the $NF{\kappa}B$-dependent transcriptional activity. Conclusion : These results suggest that PM2.5 stimulates the immediate production of RNS, leading to the activation of $NF{\kappa}B$ in the pulmonary epithelium.
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