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)~54권4호(2021) |수록논문 수 : 4,502
BMB Reports
54권4호(2021년) 수록논문
최근 권호 논문
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KCI등재 SCI SCOPUS

1Regulation of polyubiquitin genes to meet cellular ubiquitin requirement

저자 : Seung-woo Han , Byung-kwon Jung , Kwon-yul Ryu

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 54권 4호 발행 연도 : 2021 페이지 : pp. 189-195 (7 pages)

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Ubiquitin (Ub) is one of the proteins that are highly conserved from yeast to humans. It is an essential core unit of the welldefined post-translational modification, called ubiquitination, which is involved in a variety of biological processes. In metazoans, Ub is encoded by two monoubiquitin genes and two polyubiquitin genes, in which a single Ub is fused to a ribosomal protein or Ub coding units are arranged in tandem repeats. In mice, polyubiquitin genes (Ubb and Ubc) play a pivotal role to meet the requirement of cellular Ub pools during embryonic development. In addition, expression levels of polyubiquitin genes are increased to adapt to environmental stimuli such as oxidative, heat-shock, and proteotoxic stress. Several researchers have reported about the perturbation of Ub pools through genetic alteration or exogenous Ub delivery using diverse model systems. To study Ub pool changes in a physiologically relevant manner, changing Ub pools via the regulation of endogenous polyubiquitin gene expression has recently been introduced. Furthermore, to understand the regulation of polyubiquitin gene expression more precisely, cis-acting elements and trans-acting factors, which are regulatory components of polyubiquitin genes, have been analyzed. In this review, we discuss how the role of polyubiquitin genes has been studied during the past decade, especially focusing on their regulation. [BMB Reports 2021; 54(4): 189-195]

KCI등재 SCI SCOPUS

2The blood cerebrospinal fluid barrier orchestrates immunosurveillance, immunoprotection, and immunopathology in the central nervous system

저자 : Maria Ayub , Hee Kyung Jin , Jae-sung Bae

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 54권 4호 발행 연도 : 2021 페이지 : pp. 196-202 (7 pages)

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Once characterized as an immune privileged area, recent scientific advances have demonstrated that the central nervous system (CNS) is both immunologically active and a specialized site. The anatomical and cellular features of the brain barriers, the glia limitans, and other superficial coverings of the CNS endow the brain with specificity for immune cell entry and other macro- and micro-elements to the brain. Cellular trafficking via barriers comprised of tightly junctioned non-fenestrated endothelium or tightly regulated fenestrated epithelium results in different phenotypic and cellular changes in the brain, that is, inflammatory versus regulatory changes. Based on emerging evidence, we described the unique ability of the blood cerebrospinal fluid barrier (BCSFB) to recruit, skew, and suppress immune cells. Additionally, we sum up the current knowledge on both cellular and molecular mechanisms governed by the choroid plexus and the cerebrospinal fluid at the BCSFB for immunosurveillance, immunoprotection, and immunopathology. [BMB Reports 2021; 54(4): 196-202]

KCI등재 SCI SCOPUS

3Lysophosphatidylcholine aggravates contact hypersensitivity by promoting neutrophil infiltration and IL17 expression

저자 : Mi Hye Song , Anupriya Gupta , Hye One Kim , Kwonik Oh

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 54권 4호 발행 연도 : 2021 페이지 : pp. 203-208 (6 pages)

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Lysophosphatidylcholine (LPC) is a bioactive lysolipid known to contribute to the development of lung allergic diseases. However, it remains unknown whether LPC possesses proinflammatory properties in the skin as well. Here, we investigated this issue by injection of LPC into the murine contact hypersensitivity (CHS) model induced by 2,4-dinitrofluorobenzene (DNFB). LPC increased the expression of IL17, recruited more neutrophils, and eventually aggravated the CHS in the skins. Moreover, the effects of LPC diminished after neutralizing IL17 or depleting neutrophils. Mechanistically, LPC upregulated not only IL17 but also CXCL1 and CXCL2 in a G2A-dependent manner. Taken together, our study demonstrated that the upregulation of LPC could contribute to allergic skin inflammation by increasing IL17 expression and neutrophil recruitment via G2A receptor. [BMB Reports 2021; 54(4): 203-208]

KCI등재 SCI SCOPUS

4CD1d deficiency limits tolerogenic properties of peritoneal macrophages

저자 : Fathihah Basri , Sundo Jung , Se Hoon Park , Se-ho Park

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 54권 4호 발행 연도 : 2021 페이지 : pp. 209-214 (6 pages)

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Invariant natural killer T (iNKT) cells are involved in various autoimmune diseases. Although iNKT cells are arthritogenic, transforming growth factor beta (TGFβ)-treated tolerogenic peritoneal macrophages (Tol-pMψ) from wild-type (WT) mice are more tolerogenic than those from CD1d knock-out iNKT cell-deficient mice in a collagen-induced arthritis (CIA) model. The underlying mechanism by which pMφ can act as tolerogenic antigen presenting cells (APCs) is currently unclear. To determine cellular mechanisms underlying CD1d-dependent tolerogenicity of pMφ, in vitro and in vivo characteristics of pMφ were investigated. Unlike dendritic cells or splenic Mφ, pMφ from CD1d+/- mice showed lower expression levels of costimulatory molecule CD86 and produced lower amounts of inflammatory cytokines upon lipopolysaccharide (LPS) stimulation compared to pMφ from CD1d-deficient mice. In a CIA model of CD1d-deficient mice, adoptively transferred pMφ from WT mice reduced the severity of arthritis. However, pMφ from CD1d-deficient mice were unable to reduce the severity of arthritis. Hence, the tolerogenicity of pMφ is a cell-intrinsic property that is probably conferred by iNKT cells during pMφ development rather than by interactions of pMφ with iNKT cells during antigen presentation to cognate T cells. [BMB Reports 2021; 54(4): 209-214]

KCI등재 SCI SCOPUS

5Lin28a ameliorates glucotoxicity-induced β-cell dysfunction and apoptosis

저자 : Yeo Jin Hwang , Gwon-soo Jung , Wonbae Jeon , Kyeong-min Lee

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 54권 4호 발행 연도 : 2021 페이지 : pp. 215-220 (6 pages)

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An excessive and prolonged increase in glucose levels causes β-cell dysregulation, which is accompanied by impaired insulin synthesis and secretion, a condition known as glucotoxicity. Although it is known that both Lin28a and Lin28b regulate glucose metabolism, other molecular mechanisms that may protect against glucotoxicity are poorly understood. We investigated whether Lin28a overexpression can improve glucotoxicityinduced β-cell dysregulation in INS-1 and primary rat islet cells. INS-1, a rat insulinoma cell line was cultured and primary rat islet cells were isolated from SD-rats. To define the effect of Lin28a in chronic high glucose-induced β-cell dysregulation, we performed several in vitro and ex-vivo experiments. Chronic exposure to high glucose led to a downregulation of Lin28a mRNA and protein expression, followed by a decrease in insulin mRNA expression and secretion in β-cells. The mRNA and protein expression levels of PDX-1 and BETA2, were reduced; The levels of apoptotic factors, including c-caspase3 and the Bax/Bcl-2 ratio, were increased due to glucotoxicity. Adenovirusmediated Lin28a overexpression in β-cells reversed the glucotoxicity- induced reduction of insulin secretion and insulin mRNA expression via regulation of β-cell-enriched transcription factors such as PDX-1 and BETA2. Adenovirus-mediated overexpression of Lin28a downregulated the glucotoxicity-induced upregulation of c-caspase3 levels and the Bax/Bcl-2 ratio, while inhibition of endogenous Lin28a by small interfering RNA resulted in their up-regulation. Lin28a counteracted glucotoxicity-induced downregulation of p-Akt and p-mTOR. Our results suggest that Lin28a protects pancreatic β-cells from glucotoxicity through inhibition of apoptotic factors via the PI3 kinase/Akt/mTOR pathway. [BMB Reports 2021; 54(4): 215-220]

KCI등재 SCI SCOPUS

6Gluconeogenic signals regulate hepcidin gene expression via a CRBN-KLF15 axis

저자 : Jeong-rang Jo , Sung-eun Lee , Seungwon An , Balachandar Nedumaran , Swati Ghosh , Keun-gyu Park , Yong Deuk Kim

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 54권 4호 발행 연도 : 2021 페이지 : pp. 221-226 (6 pages)

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Hepcidin (HAMP) is synthesized in the liver. It is a key ironregulatory hormone that controls systemic iron homeostasis. Cereblon (CRBN) and Kruppel-like factor 15 (KLF15) are known to regulate diverse physiological functions. In this study, we investigated the role of CRBN on hepatic hepcidin gene expression and production under gluconeogenic stimuli. Fasted mice as well as forskolin (FSK)- and glucagon (GLU)-treated mice had reduced serum iron levels but increased expression levels of hepatic Crbn and Klf15 and hepcidin secretion. MicroRNA (miRNA) expression analysis of fasted and Ad-Crbninfected mice revealed significant reduction of microRNA-639 (miR-639). Hepatic overexpression of Crbn elevated hepcidin expression and production along with Klf15 gene expression, whereas knockdown of Crbn and Klf15 markedly decreased FSK- and fasting-mediated induction of hepcidin gene expression and its biosynthesis in mouse livers and primary hepatocytes. Moreover, expression of KLF15 significantly increased the activity of hepcidin reporter gene. It was exclusively dependent on the KLF15-binding site identified within the hepcidin gene promoter. Overall, this study demonstrates that CRBN and KLF15 are novel mediators of gluconeogenic signal-induced hepcidin gene expression and production. Thus, CRBN and KLF15 might be novel potential therapeutic targets to intervene metabolic dysfunction. [BMB Reports 2021; 54(4): 221-226]

KCI등재 SCI SCOPUS

7Mitochondrial dysfunction induced by callyspongiolide promotes autophagy-dependent cell death

저자 : Soohyun Lee , Yoonjeong Jeong , Jae-seok Roe , Hoyoung Huh , Sang Hoon Paik , Jaewhan Song

발행기관 : 생화학분자생물학회(구 한국생화학분자생물학회) 간행물 : BMB Reports 54권 4호 발행 연도 : 2021 페이지 : pp. 227-232 (6 pages)

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Callyspongiolide is a marine macrolide known to induce caspaseindependent cancer cell death. While its toxic effects have been known, the mechanism leading to cell death is yet to be identified. We report that Callyspongiolide R form at C-21 (cally2R) causes mitochondrial dysfunction by inhibiting mitochondrial complex I or II, leading to a disruption of mitochondrial membrane potential and a deprivation of cellular energy. Subsequently, we observed, using electron microscopy, a drastic formation of autophagosome and mitophagy. Supporting these data, LC3, an autophagosome marker, was shown to co-localize with LAMP2, a lysosomal protein, showing autolysosome formation. RNA sequencing results indicated the induction of hypoxia and blocking of EGF-dependent pathways, which could be caused by induction of autophagy. Furthermore, mTOR and AKT pathways preventing autophagy were repressed while AMPK was upregulated, supporting autophagosome progress. Finally, the combination of cally2R with known anti-cancer drugs, such as gefitinib, sorafenib, and rapamycin, led to synergistic cell death, implicating potential therapeutic applications of callyspongiolide for future treatments. [BMB Reports 2021; 54(4): 227-232]

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(2006)홍길동 외 1명심리학41회 피인용

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