간행물

BMB Reports update

Biochemistry and Molecular Biology Reports

  • : 생화학분자생물학회(구 한국생화학분자생물학회)
  • : 자연과학분야  >  화학
  • : KCI등재
  • : SCI,SCOPUS
  • : 연속간행물
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  • : 1976-6696
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  • : Korean Biochemical Journal(~1994)→Journal of Biochemistry and Molecular Biology(1995~)→Biochemistry and Molecurar Biology Reports(2008~)

수록정보
수록범위 : 1권1호(1968)~53권2호(2020) |수록논문 수 : 4,392
BMB Reports
53권2호(2020년 02월) 수록논문
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KCI등재 SCI SCOPUS

1Impact of mesenchymal stem cell senescence on inflammaging

저자 : Byung-chul Lee , Kyung-rok Yu

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 65-73 (9 pages)

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Life expectancy has dramatically increased around the world over the last few decades, and staying healthier longer, without chronic disease, has become an important issue. Although understanding aging is a grand challenge, our understanding of the mechanisms underlying the degeneration of cell and tissue functions with age and its contribution to chronic disease has greatly advanced during the past decade. As our immune system alters with aging, abnormal activation of immune cells leads to imbalance of innate and adaptive immunity and develops a persistent and mild systemic inflammation, inflammaging. With their unique therapeutic properties, such as immunomodulation and tissue regeneration, mesenchymal stem cells (MSCs) have been considered to be a promising source for treating autoimmune disease or as anti-aging therapy. Although direct evidence of the role of MSCs in inflammaging has not been thoroughly studied, features reported in senescent MSCs or the aging process of MSCs are associated with inflammaging; MSC niche-driven skewing of hematopoiesis toward the myeloid lineage or oncogenesis, production of pro-inflammatory cytokines, and weakening their modulative property on macrophage polarization, which plays a central role on inflammaging development. This review explores the role of senescent MSCs as an important regulator for onset and progression of inflammaging and as an effective target for anti-aging strategies. [BMB Reports 2020; 53(2): 65-73]

KCI등재 SCI SCOPUS

2Traction force microscopy for understanding cellular mechanotransduction

저자 : Sung Sik Hur , Ji Hoon Jeong , Myung Jin Ban , Jae Hong Park , Jeong Kyo Yoon , Yongsung Hwang

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 74-81 (8 pages)

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Under physiological and pathological conditions, mechanical forces generated from cells themselves or transmitted from extracellular matrix (ECM) through focal adhesions (FAs) and adherens junctions (AJs) are known to play a significant role in regulating various cell behaviors. Substantial progresses have been made in the field of mechanobiology towards novel methods to understand how cells are able to sense and adapt to these mechanical forces over the years. To address these issues, this review will discuss recent advancements of traction force microscopy (TFM), intracellular force microscopy (IFM), and monolayer stress microscopy (MSM) to measure multiple aspects of cellular forces exerted by cells at cell-ECM and cell-cell junctional intracellular interfaces. We will also highlight how these methods can elucidate the roles of mechanical forces at interfaces of cell-cell/cell-ECM in regulating various cellular functions. [BMB Reports 2020; 53(2): 74-81]

KCI등재 SCI SCOPUS

3Circular RNA hsa_circ_0075828 promotes bladder cancer cell proliferation through activation of CREB1

저자 : Chengle Zhuang , Xinbo Huang , Jing Yu , Yaoting Gui

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 82-87 (6 pages)

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Circular RNAs (circRNAs), one kind of non-coding RNA, have been reported as critical regulators for modulating gene expression in cancer. In this study, microarray analysis was used to screen circRNA expression profiles of bladder cancer (BC) 5637 cells, T24 cells and normal control SV-HUC-1 cells. The data from the microarray showed that hsa_circ_0075828 (named circCASC15) was most highly expressed in 5637 and T24 cells. circCASC15 was highly expressed in BC tissues and cells. Overexpression of circCASC15 was closely associated with BC tumor stage and promoted cell proliferation significantly in vitro and in vivo. Mechanistically, circCASC15 could act as miR-1224-5p sponge to activate the expression of CREB1 to promote cell proliferation in BC. In short, circCASC15 promotes cell proliferation in BC, which might be a new molecular target for BC diagnosis and therapy. [BMB Reports 2020; 53(2): 82-87]

KCI등재 SCI SCOPUS

4Overcoming multidrug resistance by activating unfolded protein response of the endoplasmic reticulum in cisplatin-resistant A2780/CisR ovarian cancer cells

저자 : Euitaek Jung , Dongsoo Koh , Yoongho Lim , Soon Young Shin , Young Han Lee

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 88-93 (6 pages)

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Cisplatin is a widely used anti-cancer agent. However, the effectiveness of cisplatin has been limited by the commonly developed drug resistance. This study aimed to investigate the potential effects of endoplasmic reticulum (ER) stress to overcome drug resistance using the cisplatin-resistant A2780/CisR ovarian cancer cell model. The synthetic chalcone derivative (E)-3-(3,5-dimethoxyphenyl)-1-(2-methoxyphenyl)prop- 2-en-1-one (named DPP23) is an ER stress inducer. We found that DPP23 triggered apoptosis in both parental cisplatinsensitive A2780 and cisplatin-resistant A2780/CisR ovarian cancer cells due to activation of reactive oxygen species (ROS)-mediated unfolded protein response (UPR) pathway in the endoplasmic reticulum. This result suggests that ROSmediated UPR activation is potential in overcoming drug resistance. DPP23 can be used as a target pharmacophore for the development of novel chemotherapeutic agents capable of overcoming drug resistance in cancer cells, particularly ovarian cancer cells. [BMB Reports 2020; 53(2): 88-93]

KCI등재 SCI SCOPUS

5Functional analysis of RNA motifs essential for BC200 RNA-mediated translational regulation

저자 : Seonghui Jang , Heegwon Shin , Younghoon Lee

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 94-99 (6 pages)

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Brain cytoplasmic 200 RNA (BC200 RNA) is proposed to act as a local translational modulator by inhibiting translation after being targeted to neuronal dendrites. However, the mechanism by which BC200 RNA inhibits translation is not fully understood. Although a detailed functional analysis of RNA motifs is essential for understanding the BC200 RNA-mediated translation-inhibition mechanism, there is little relevant research on the subject. Here, we performed a systematic domain-dissection analysis of BC200 RNA to identify functional RNA motifs responsible for its translationalinhibition activity. Various RNA variants were assayed for their ability to inhibit translation of luciferase mRNA in vitro. We found that the 111-200-nucleotide region consisting of part of the Alu domain as well as the A/C-rich domain (consisting of both the A-rich and C-rich domains) is most effective for translation inhibition. Surprisingly, we also found that individual A-rich, A/C-rich, and Alu domains can enhance translation but at different levels for each domain, and that these enhancing effects manifest as cap-dependent translation. [BMB Reports 2020; 53(2): 94-99]

KCI등재 SCI SCOPUS

6Heterogeneity in liver histopathology is associated with GSK-3β activity and mitochondrial dysfunction in end-stage diabetic rats on differential diets

저자 : Jun-ho Lee , Soo-bong Choi , Dong-jun Sung , Mingli Jin , Ju-han Lee , Ji-young Mun , Tae-sook Hwang , Sang-don Han , Young-tae Ro , Sung-young Kim , Jueng-soo You , Inja Lim , Yun-hee Noh

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 100-105 (6 pages)

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While liver histopathology is heterogeneous in diabetes, the underlying mechanisms remain unclear. We investigated whether glycemic variation resulting from differential diets can induce heterogeneity in diabetic liver and the underlying molecular mechanisms. We generated end-stage non-obese diabetic model rats by subtotal-pancreatectomy in male Sprague- Dawley rats and ad libitum diet for 7 weeks (n = 33). The rats were then divided into three groups, and fed a standard- or a low-protein diet (18 or 6 kcal%, respectively), for another 7 weeks: to maintain hyperglycemia, 11 rats were fed ad libitum (18AL group); to achieve euglycemia, 11 were calorierestricted (18R group), and 11 were both calorie- and proteinrestricted with the low-protein diet (6R group). Overnightfasted liver samples were collected after the differential diets together with sham-control (18S group), and histology and molecular changes were compared. Hyperglycemic-18AL showed glycogenic hepatopathy (GH) without steatosis, with the highest GSK-3β inactivation because of Akt activation during hyperglycemia; mitochondrial function was not impaired, compared to the 18S group. Euglycemic-18R showed neither GH nor steatosis, with intermediate GSK-3β activation and mitochondrial dysfunction. However, euglycemic-6R showed both GH and steatosis despite the highest GSK-3β activity and no molecular evidence of increased lipogenesis or decreased ApoB expression, where mitochondrial dysfunction was highest among the groups. In conclusion, heterogeneous liver histopathology developed in end-stage non-obese diabetic rats as the glycemic levels varied with differential diets, in which protein content in the diets as well as glycemic levels differentially influenced GSK-3β activity and mitochondrial function in insulin-deficient state. [BMB Reports 2020; 53(2): 100-105]

KCI등재 SCI SCOPUS

7PEP-1-GLRX1 protein exhibits anti-inflammatory effects by inhibiting the activation of MAPK and NF-κB pathways in Raw 264.7 cells

저자 : Min Jea Shin , Dae Won Kim , Yeon Joo Choi , Hyun Ju Cha , Sung Ho Lee , Sunghou Lee , Jinseu Park , Kyu Hyung Han , Won Sik Eum , Soo Young Choi

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 106-111 (6 pages)

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Glutaredoxin 1 (GLRX1) has been recognized as an important regulator of redox signaling. Although GLRX1 plays an essential role in cell survival as an antioxidant protein, the function of GLRX1 protein in inflammatory response is still under investigation. Therefore, we wanted to know whether transduced PEP-1-GLRX1 protein inhibits lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced inflammation. In LPS-exposed Raw 264.7 cells, PEP-1-GLRX1 inhibited cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), activation of mitogen activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-κB) expression levels. In a TPA-induced mouse-ear edema model, topically applied PEP-1-GLRX1 transduced into ear tissues and significantly ameliorated ear edema. Our data reveal that PEP-1-GLRX1 attenuates inflammation in vitro and in vivo, suggesting that PEP-1-GLRX1 may be a potential therapeutic protein for inflammatory diseases. [BMB Reports 2020; 53(2): 106-111]

KCI등재 SCI SCOPUS

8Methylated-UHRF1 and PARP1 interaction is critical for homologous recombination

저자 : Ja Young Hahm , Joo-young Kang , Jin Woo Park , Hyeonsoo Jung , Sang-beom Seo

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 112-117 (6 pages)

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A recent study suggested that methylation of ubiquitin-like with PHD and RING finger domain 1 (UHRF1) is regulated by SET7 and lysine-specific histone demethylase 1A (LSD1) and is essential for homologous recombination (HR). The study demonstrated that SET7-mediated methylation of UHRF1 promotes polyubiquitination of proliferating cell nuclear antigen (PCNA), inducing HR. However, studies on mediators that interact with and recruit UHRF1 to damaged lesions are needed to elucidate the mechanism of UHRF1 methylationinduced HR. Here, we identified that poly [ADP-ribose] polymerase 1 (PARP1) interacts with damage-induced methylated UHRF1 specifically and mediates UHRF1 to induce HR progression. Furthermore, cooperation of UHRF1-PARP1 is essential for cell viability, suggesting the importance of the interaction of UHRF1-PARP1 for damage tolerance in response to damage. Our data revealed that PARP1 mediates the HR mechanism, which is regulated by UHRF1 methylation. The data also indicated the significant role of PARP1 as a mediator of UHRF1 methylation-correlated HR pathway. [BMB Reports 2020; 53(2): 112-117]

KCI등재 SCI SCOPUS

9Characterization of human cardiac mesenchymal stromal cells and their extracellular vesicles comparing with human bone marrow derived mesenchymal stem cells

저자 : In Sook Kang , Joowon Suh , Mi-ni Lee , Chaeyoung Lee , Jing Jin , Changjin Lee , Young Il Yang , Yangsoo Jang , Goo Taeg Oh

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 53권 2호 발행 연도 : 2020 페이지 : pp. 118-123 (6 pages)

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Cardiac regeneration with adult stem-cell (ASC) therapy is a promising field to address advanced cardiovascular diseases. In addition, extracellular vesicles (EVs) from ASCs have been implicated in acting as paracrine factors to improve cardiac functions in ASC therapy. In our work, we isolated human cardiac mesenchymal stromal cells (h-CMSCs) by means of three-dimensional organ culture (3D culture) during ex vivo expansion of cardiac tissue, to compare the functional efficacy with human bone-marrow derived mesenchymal stem cells (h-BM-MSCs), one of the actively studied ASCs. We characterized the h-CMSCs as CD90low, c-kitnegative, CD105positive phenotype and these cells express NANOG, SOX2, and GATA4. To identify the more effective type of EVs for angiogenesis among the different sources of ASCs, we isolated EVs which were derived from CMSCs with either normoxic or hypoxic condition and BM-MSCs. Our in vitro tube-formation results demonstrated that the angiogenic effects of EVs from hypoxia-treated CMSCs (CMSC-Hpx EVs) were greater than the well-known effects of EVs from BM-MSCs (BM-MSC EVs), and these were even comparable to human vascular endothelial growth factor (hVEGF), a potent angiogenic factor. Therefore, we present here that CD90lowc-kitnegativeCD105positive CMSCs under hypoxic conditions secrete functionally superior EVs for in vitro angiogenesis. Our findings will allow more insights on understanding myocardial repair. [BMB Reports 2020; 53(2): 118-123]

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