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생화학분자생물학회> BMB Reports> Acetate decreases PVR/CD155 expression via PI3K/AKT pathway in cancer cells

KCI등재SCISCOUPUS

Acetate decreases PVR/CD155 expression via PI3K/AKT pathway in cancer cells

Na Ly Tran , In Kyu Lee , Jungkyun Choi , Sang-heon Kim , Seung Ja Oh
  • : 생화학분자생물학회
  • : BMB Reports 54권8호
  • : 연속간행물
  • : 2021년 08월
  • : 431-436(6pages)
BMB Reports

DOI


목차

INTRODUCTION
RESULTS
DISCUSSION
MATERIALS AND METHODS
ACKNOWLEDGEMENTS
CONFLICTS OF INTEREST
REFERENCES

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In recent years, restoring anti-tumor immunity has garnered a growing interest in cancer treatment. As potential therapeutics, immune checkpoint inhibitors have demonstrated benefits in many clinical studies. Although various methods have been applied to suppress immune checkpoints to boost anti-tumor immunity, including the use of immune checkpoint inhibitors, there are still unmet clinical needs to improve the response rate of cancer treatment. Here, we show that acetate can suppress the expression of poliovirus receptor (PVR/CD155), a ligand for immune checkpoint, in colon cancer cells. We demonstrated that acetate treatment could enhance effector responses of CD8+ T cells by decreasing the expression of PVR/CD155 in cancer cells. We also found that acetate could reduce the expression of PVR/CD155 by deactivating the PI3K/AKT pathway. These results demonstrate that acetate-mediated expression of PVR/CD155 in cancer cells might potentiate the anti-tumor immunity in the microenvironment of cancer. Our findings indicate that maintaining particular acetate concentrations could be a complementary strategy in current cancer treatment. [BMB Reports 2021; 54(8): 431-436]

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간행물정보

  • : 자연과학분야  > 화학
  • : KCI등재
  • : SCI,SCOPUS
  • : 월간
  • : 1976-6696
  • : 1976-670X
  • : 학술지
  • : 연속간행물
  • : 1968-2021
  • : 4538


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KCI등재 SCI SCOPUS

1The trinity of ribosome-associated quality control and stress signaling for proteostasis and neuronal physiology

저자 : Jumin Park , Jongmin Park , Jongbin Lee , Chunghun Lim

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 9호 발행 연도 : 2021 페이지 : pp. 439-450 (12 pages)

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Translating ribosomes accompany co-translational regulation of nascent polypeptide chains, including subcellular targeting, protein folding, and covalent modifications. Ribosome-associated quality control (RQC) is a co-translational surveillance mechanism triggered by ribosomal collisions, an indication of atypical translation. The ribosome-associated E3 ligase ZNF598 ubiquitinates small subunit proteins at the stalled ribosomes. A series of RQC factors are then recruited to dissociate and triage aberrant translation intermediates. Regulatory ribosomal stalling may occur on endogenous transcripts for quality gene expression, whereas ribosomal collisions are more globally induced by ribotoxic stressors such as translation inhibitors, ribotoxins, and UV radiation. The latter are sensed by ribosome-associated kinases GCN2 and ZAKα, activating integrated stress response (ISR) and ribotoxic stress response (RSR), respectively. Hierarchical crosstalks among RQC, ISR, and RSR pathways are readily detectable since the collided ribosome is their common substrate for activation. Given the strong implications of RQC factors in neuronal physiology and neurological disorders, the interplay between RQC and ribosome-associated stress signaling may sustain proteostasis, adaptively determine cell fate, and contribute to neural pathogenesis. The elucidation of underlying molecular principles in relevant human diseases should thus provide unexplored therapeutic opportunities. [BMB Reports 2021; 54(9): 439-450]

KCI등재 SCI SCOPUS

2Emerging roles of PHLPP phosphatases in metabolism

저자 : Jong-ho Cha , Yelin Jeong , Ah-reum Oh , Sang Bae Lee , Soon-sun Hong , Kyeongjin Kim

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 9호 발행 연도 : 2021 페이지 : pp. 451-457 (7 pages)

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Over the last decades, research has focused on the role of pleckstrin homology (PH) domain leucine-rich repeat protein phosphatases (PHLPPs) in regulating cellular signaling via PI3K/Akt inhibition. The PKB/Akt signaling imbalances are associated with a variety of illnesses, including various types of cancer, inflammatory response, insulin resistance, and diabetes, demonstrating the relevance of PHLPPs in the prevention of diseases. Furthermore, identification of novel substrates of PHLPPs unveils their role as a critical mediator in various cellular processes. Recently, researchers have explored the increasing complexity of signaling networks involving PHLPPs whereby relevant information of PHLPPs in metabolic diseases was obtained. In this review, we discuss the current knowledge of PHLPPs on the well-known substrates and metabolic regulation, especially in liver, pancreatic beta cell, adipose tissue, and skeletal muscle in relation with the stated diseases. Understanding the context-dependent functions of PHLPPs can lead to a promising treatment strategy for several kinds of metabolic diseases. [BMB Reports 2021; 54(9): 451-457]

KCI등재 SCI SCOPUS

3Tat-CIAPIN1 protein prevents against cytokine-induced cytotoxicity in pancreatic RINm5Fβ-cells

저자 : Hyeon Ji Yeo , Min Jea Shin , Dae Won Kim , Hyeok Yil Kwon , Won Sik Eum , Soo Young Choi

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 9호 발행 연도 : 2021 페이지 : pp. 458-463 (6 pages)

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Cytokines activate inflammatory signals and are major mediators in progressiveβ-cell damage, which leads to type 1 diabetes mellitus. We recently showed that the cell-permeable Tat-CIAPIN1 fusion protein inhibits neuronal cell death induced by oxidative stress. However, how the Tat-CIAPIN1 protein affects cytokine- inducedβ-cell damage has not been investigated yet. Thus, we assessed whether the Tat-CIAPIN1 protein can protect RINm5Fβ-cells against cytokine-induced cytotoxicity. In cytokineexposed RINm5Fβ-cells, the transduced Tat-CIAPIN1 protein elevated cell survivals and reduced reactive oxygen species (ROS) and DNA fragmentation levels. The Tat-CIAPIN1 protein reduced mitogen-activated protein kinases (MAPKs) and NF-βB activation levels and elevated Bcl-2 protein, whereas Bax and cleaved Caspase-3 proteins were decreased by this fusion protein. Thus, the protection of RINm5Fβ-cells by the Tat-CIAPIN1 protein against cytokine-induced cytotoxicity can suggest that the Tat-CIAPIN1 protein might be used as a therapeutic inhibitor against RINm5Fβ-cell damage. [BMB Reports 2021; 54(9): 458-463]

KCI등재 SCI SCOPUS

4Stage specific transcriptome profiles at cardiac lineage commitment during cardiomyocyte differentiation from mouse and human pluripotent stem cells

저자 : Sung Woo Cho , Hyoung Kyu Kim , Ji Hee Sung , Jin Han

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 9호 발행 연도 : 2021 페이지 : pp. 464-469 (6 pages)

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Cardiomyocyte differentiation occurs through complex and finely regulated processes including cardiac lineage commitment and maturation from pluripotent stem cells (PSCs). To gain some insight into the genome-wide characteristics of cardiac lineage commitment, we performed transcriptome analysis on both mouse embryonic stem cells (mESCs) and human induced PSCs (hiPSCs) at specific stages of cardiomyocyte differentiation. Specifically, the gene expression profiles and the protein- protein interaction networks of the mESC-derived plateletderived growth factor receptor-alpha (PDGFRα)+ cardiac lineagecommitted cells (CLCs) and hiPSC-derived kinase insert domain receptor (KDR)+ and PDGFRα+ cardiac progenitor cells (CPCs) at cardiac lineage commitment were compared with those of mesodermal cells and differentiated cardiomyocytes. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that the genes significantly upregulated at cardiac lineage commitment were associated with responses to organic substances and external stimuli, extracellular and myocardial contractile components, receptor binding, gated channel activity, PI3K-AKT signaling, and cardiac hypertrophy and dilation pathways. Protein-protein interaction network analysis revealed that the expression levels of genes that regulate cardiac maturation, heart contraction, and calcium handling showed a consistent increase during cardiac differentiation; however, the expression levels of genes that regulate cell differentiation and multicellular organism development decreased at the cardiac maturation stage following lineage commitment. Additionally, we identified for the first time the protein-protein interaction network connecting cardiac development, the immune system, and metabolism during cardiac lineage commitment in both mESC-derived PDGFRα+ CLCs and hiPSC-derived KDR+PDGFRα+ CPCs. These findings shed light on the regulation of cardiac lineage commitment and the pathogenesis of cardiometabolic diseases. [BMB Reports 2021; 54(9): 464-469]

KCI등재 SCI SCOPUS

5Low-dose metronomic doxorubicin inhibits mobilization and differentiation of endothelial progenitor cells through REDD1-mediated VEGFR-2 downregulation

저자 : Minsik Park , Ji Yoon Kim , Joohwan Kim , Jeong-hyung Lee , Young-guen Kwon , Young-myeong Kim

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 9호 발행 연도 : 2021 페이지 : pp. 470-475 (6 pages)

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Low-dose metronomic chemotherapy has been introduced as a less toxic and effective strategy to inhibit tumor angiogenesis, but its anti-angiogenic mechanism on endothelial progenitor cells (EPCs) has not been fully elucidated. Here, we investigated the functional role of regulated in development and DNA damage response 1 (REDD1), an endogenous inhibitor of mTORC1, in low-dose doxorubicin (DOX)-mediated dysregulation of EPC functions. DOX treatment induced REDD1 expression in bone marrow mononuclear cells (BMMNCs) and subsequently reduced mTORC1-dependent translation of endothelial growth factor (VEGF) receptor (Vegfr)-2 mRNA, but not that of the mRNA transcripts for Vegfr-1, epidermal growth factor receptor, and insulin-like growth factor-1 receptor. This selective event was a risk factor for the inhibition of BMMNC differentiation into EPCs and their angiogenic responses to VEGF-A, but was not observed in Redd1-deficient BMMNCs. Low-dose metronomic DOX treatment reduced the mobilization of circulating EPCs in B16 melanoma-bearing wild-type but not Redd1-deficient mice. However, REDD1 overexpression inhibited the differentiation and mobilization of EPCs in both wild-type and Redd1- deficient mice. These data suggest that REDD1 is crucial for metronomic DOX-mediated EPC dysfunction through the translational repression of Vegfr-2 transcript, providing REDD1 as a potential therapeutic target for the inhibition of tumor angiogenesis and tumor progression. [BMB Reports 2021; 54(9): 470-475]

KCI등재 SCI SCOPUS

6Perilipin 5 is a novel target of nuclear receptor LRH-1 to regulate hepatic triglycerides metabolism

저자 : Rubee Pantha , Jae-ho Lee , Jae-hoon Bae , Eun Hee Koh , Minsang Shin , Dae-kyu Song , Seung-soon Im

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 9호 발행 연도 : 2021 페이지 : pp. 476-481 (6 pages)

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Liver receptor homolog-1 (LRH-1) has emerged as a regulator of hepatic glucose, bile acid, and mitochondrial metabolism. However, the functional mechanism underlying the effect of LRH-1 on lipid mobilization has not been addressed. This study investigated the regulatory function of LRH-1 in lipid metabolism in maintaining a normal liver physiological state during fasting. The Lrh-1f/f and LRH-1 liver-specific knockout (Lrh-1LKO) mice were either fed or fasted for 24 h, and the liver and serum were isolated. The livers were used for qPCR, western blot, and histological analysis. Primary hepatocytes were isolated for immunocytochemistry assessments of lipids. During fasting, the Lrh-1LKO mice showed increased accumulation of triglycerides in the liver compared to that in Lrh-1f/f mice. Interestingly, in the Lrh-1LKO liver, decreases in perilipin 5 (PLIN5) expression and genes involved inβ-oxidation were observed. In addition, the LRH-1 agonist dialauroylphosphatidylcholine also enhanced PLIN5 expression in human cultured HepG2 cells. To identify new target genes of LRH-1, these findings directed us to analyze the Plin5 promoter sequence, which revealed -1620/-1614 to be a putative binding site for LRH-1. This was confirmed by promoter activity and chromatin immunoprecipitation assays. Additionally, fasted Lrh-1f/f primary hepatocytes showed increased co-localization of PLIN5 in lipid droplets (LDs) compared to that in fasted Lrh-1LKO primary hepatocytes. Overall, these findings suggest that PLIN5 might be a novel target of LRH-1 to mobilize LDs, protect the liver from lipid overload, and manage the cellular needs during fasting. [BMB Reports 2021; 54(9): 476-481]

KCI등재 SCI SCOPUS

7IRF2 enhances RANKL-induced osteoclast differentiation via regulating NF-κB/NFATc1 signaling

저자 : Inyoung Kim , Jung Ha Kim , Kabsun Kim , Semun Seong , Keun-bae Lee , Nacksung Kim

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 9호 발행 연도 : 2021 페이지 : pp. 482-487 (6 pages)

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Interferon regulatory factors (IRFs) play roles in various biological processes including cytokine signaling, cell growth regulation and hematopoietic development. Although it has been reported that several IRFs are involved in bone metabolism, the role of IRF2 in bone cells has not been elucidated. Here, we investigated the involvement of IRF2 in RANKL-induced osteoclast differentiation. IRF2 overexpression in osteoclast precursor cells enhanced osteoclast differentiation by regulating the expression of NFATc1, a master regulator of osteoclastogenesis. Conversely, IRF2 knockdown inhibited osteoclast differentiation and decreased the NFATc1 expression. Moreover, IRF2 increased the translocation of NF-κB subunit p65 to the nucleus in response to RANKL and subsequently induced the expression of NFATc1. IRF2 plays an important role in RANKL-induced osteoclast differentiation by regulating NF-κB/NFATc1 signaling pathway. Taken together, we demonstrated the molecular mechanism of IRF2 in osteoclast differentiation, and provide a molecular basis for potential therapeutic targets for the treatment of bone diseases characterized by excessive bone resorption. [BMB Reports 2021; 54(9): 482-487]

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1Proprioception, the regulator of motor function

저자 : Kyeong Min Moon , Jimin Kim , Yurim Seong , Byung-chang Suh , Kyeongjin Kang , Han Kyoung Choe , Kyuhyung Kim

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 8호 발행 연도 : 2021 페이지 : pp. 393-402 (10 pages)

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In animals, proper locomotion is crucial to find mates and foods and avoid predators or dangers. Multiple sensory systems detect external and internal cues and integrate them to modulate motor outputs. Proprioception is the internal sense of body position, and proprioceptive control of locomotion is essential to generate and maintain precise patterns of movement or gaits. This proprioceptive feedback system is conserved in many animal species and is mediated by stretch-sensitive receptors called proprioceptors. Recent studies have identified multiple proprioceptive neurons and proprioceptors and their roles in the locomotion of various model organisms. In this review we describe molecular and neuronal mechanisms underlying proprioceptive feedback systems in C. elegans, Drosophila, and mice. [BMB Reports 2021; 54(8): 393-402]

KCI등재SCISCOUPUS

2Perspectives on immune checkpoint ligands: expression, regulation, and clinical implications

저자 : Jihyun Moon , Yoo Min Oh , Sang-jun Ha

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 8호 발행 연도 : 2021 페이지 : pp. 403-412 (10 pages)

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In the tumor microenvironment, immune checkpoint ligands (ICLs) must be expressed in order to trigger the inhibitory signal via immune checkpoint receptors (ICRs). Although ICL expression frequently occurs in a manner intrinsic to tumor cells, extrinsic factors derived from the tumor microenvironment can fine-tune ICL expression by tumor cells or prompt non-tumor cells, including immune cells. Considering the extensive interaction between T cells and other immune cells within the tumor microenvironment, ICL expression on immune cells can be as significant as that of ICLs on tumor cells in promoting antitumor immune responses. Here, we introduce various regulators known to induce or suppress ICL expression in either tumor cells or immune cells, and concise mechanisms relevant to their induction. Finally, we focus on the clinical significance of understanding the mechanisms of ICLs for an optimized immunotherapy for individual cancer patients. [BMB Reports 2021; 54(8): 403-412]

KCI등재SCISCOUPUS

3EBP1 regulates Suv39H1 stability via the ubiquitin-proteasome system in neural development

저자 : Byeong-seong Kim , Hyo Rim Ko , Inwoo Hwang , Sung-woo Cho , Jee-yin Ahn

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 8호 발행 연도 : 2021 페이지 : pp. 413-418 (6 pages)

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ErbB3-binding protein 1 (EBP1) is a multifunctional protein associated with neural development. Loss of Ebp1 leads to upregulation of the gene silencing unit suppressor of variegation 3-9 homolog 1 (Suv39H1)/DNA (cytosine 5)-methyltransferase (DNMT1). EBP1 directly binds to the promoter region of DNMT1, repressing DNA methylation, and hence, promoting neural development. In the current study, we showed that EBP1 suppresses histone methyltransferase activity of Suv39H1 by promoting ubiquitin-proteasome system (UPS)-dependent degradation of Suv39H1. In addition, we showed that EBP1 directly interacts with Suv39H1, and this interaction is required for recruiting the E3 ligase MDM2 for Suv39H1 degradation. Thus, our findings suggest that EBP1 regulates UPS-dependent degradation of Suv39H1 to govern proper heterochromatin assembly during neural development. [BMB Reports 2021; 54(8): 413-418]

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4Nrf2 induces Ucp1 expression in adipocytes in response to β3-AR stimulation and enhances oxygen consumption in high-fat diet-fed obese mice

저자 : Seo-hyuk Chang , Jaeyool Jang , Seungjun Oh , Jung-hoon Yoon , Dong-gyu Jo , Ui Jeong Yun , Kye Won Park

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 8호 발행 연도 : 2021 페이지 : pp. 419-424 (6 pages)

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Cold-induced norepinephrine activates β3-adrenergic receptors (β3-AR) to stimulate the kinase cascade and cAMP-response element-binding protein, leading to the induction of thermogenic gene expression including uncoupling protein 1 (Ucp1). Here, we showed that stimulation of the β3-AR by its agonists isoproterenol and CL316,243 in adipocytes increased the expression of Ucp1 and Heme Oxygenase 1 (Hmox1), the principal Nrf2 target gene, suggesting the functional interaction of Nrf2 with β3-AR signaling. The activation of Nrf2 by tert-butylhydroquinone and reactive oxygen species (ROS) production by glucose oxidase induced both Ucp1 and Hmox1 expression. The increased expression of Ucp1 and Hmox1 was significantly reduced in the presence of a Nrf2 chemical inhibitor or in Nrf2-deleted (knockout) adipocytes. Furthermore, Nrf2 directly activated the Ucp1 promoter, and this required DNA regions located at -3.7 and -2.0 kb of the transcription start site. The CL316,243-induced Ucp1 expression in adipocytes and oxygen consumption in obese mice were partly compromised in the absence of Nrf2 expression. These data provide additional insight into the role of Nrf2 in β3-AR-mediated Ucp1 expression and energy expenditure, further highlighting the utility of Nrf2-mediated thermogenic stimulation as a therapeutic approach to diet-induced obesity. [BMB Reports 2021; 54(8): 419-424]

KCI등재SCISCOUPUS

5MUC1-C influences cell survival in lung adenocarcinoma Calu-3 cells after SARS-CoV-2 infection

저자 : Dongbum Kim , Sony Maharjan , Jinsoo Kim , Sangkyu Park , Jeong-a Park , Byoung Kwon Park , Younghee Lee , Hyung-joo Kwon

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 8호 발행 연도 : 2021 페이지 : pp. 425-430 (6 pages)

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces coronavirus disease 2019 (COVID-19) and may increase the risk of adverse outcomes in lung cancer patients. In this study, we investigated the expression and function of mucin 1 (MUC1) after SARS-CoV-2 infection in the lung epithelial cancer cell line Calu-3. MUC1 is a major constituent of the mucus layer in the respiratory tract and contributes to pathogen defense. SARS-CoV-2 infection induced MUC1 C-terminal subunit (MUC1-C) expression in a STAT3 activation-dependent manner. Inhibition of MUC1-C signaling increased apoptosis-related protein levels and reduced proliferation-related protein levels; however, SARS-CoV-2 replication was not affected. Together, these results suggest that increased MUC1-C expression in response to SARS-CoV-2 infection may trigger the growth of lung cancer cells, and COVID-19 may be a risk factor for lung cancer patients. [BMB Reports 2021; 54(8): 425-430]

KCI등재SCISCOUPUS

6Acetate decreases PVR/CD155 expression via PI3K/AKT pathway in cancer cells

저자 : Na Ly Tran , In Kyu Lee , Jungkyun Choi , Sang-heon Kim , Seung Ja Oh

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 8호 발행 연도 : 2021 페이지 : pp. 431-436 (6 pages)

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In recent years, restoring anti-tumor immunity has garnered a growing interest in cancer treatment. As potential therapeutics, immune checkpoint inhibitors have demonstrated benefits in many clinical studies. Although various methods have been applied to suppress immune checkpoints to boost anti-tumor immunity, including the use of immune checkpoint inhibitors, there are still unmet clinical needs to improve the response rate of cancer treatment. Here, we show that acetate can suppress the expression of poliovirus receptor (PVR/CD155), a ligand for immune checkpoint, in colon cancer cells. We demonstrated that acetate treatment could enhance effector responses of CD8+ T cells by decreasing the expression of PVR/CD155 in cancer cells. We also found that acetate could reduce the expression of PVR/CD155 by deactivating the PI3K/AKT pathway. These results demonstrate that acetate-mediated expression of PVR/CD155 in cancer cells might potentiate the anti-tumor immunity in the microenvironment of cancer. Our findings indicate that maintaining particular acetate concentrations could be a complementary strategy in current cancer treatment. [BMB Reports 2021; 54(8): 431-436]

KCI등재SCISCOUPUS

7Erratum to: Common and differential effects of docosahexaenoic acid and eicosapentaenoic acid on helper T-cell responses and associated pathways

저자 : Jaeho Lee , Yu Ri Choi , Miso Kim , Jung Mi Park , Moonjong Kang , Jaewon Oh , Chan Joo Lee , Sungha Park , Seok-min Kang , Ichiro Manabe , Soo-jin Ann , Sang-hak Lee

발행기관 : 생화학분자생물학회 간행물 : BMB Reports 54권 8호 발행 연도 : 2021 페이지 : pp. 437-437 (1 pages)

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