1,378 results match your criteria BMB reports[Journal]


Neuronal function and dysfunction of CYFIP2: from actin dynamics to early infantile epileptic encephalopathy.

BMB Rep 2019 Apr 15. Epub 2019 Apr 15.

Department of Neuroscience, College of Medicine, Korea University, Seoul 02841, South Korea; Department of Biomedical Sciences, College of Medicine, Korea University, Seoul 02841, South Korea.

The cytoplasmic FMR1-interacting protein family (CYFIP1 and CYFIP2) are evolutionarily conserved proteins originally identified as binding partners of the fragile X mental retardation protein (FMRP), a messenger RNA (mRNA)-binding protein whose loss causes the fragile X syndrome. Moreover, CYFIP is a key component of the heteropentameric WAVE regulatory complex (WRC), a critical regulator of neuronal actin dynamics. Therefore, CYFIP may play key roles in regulating both mRNA translation and actin polymerization, which are critically involved in proper neuronal development and function. Read More

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April 2019
1 Read

C-terminal Truncated HBx Reduces Doxorubicin Cytotoxicity via ABCB1 Upregulation in Huh-7 Hepatocellular Carcinoma Cells.

BMB Rep 2019 Apr 15. Epub 2019 Apr 15.

Department of Molecular Biology, College of Natural Science, Pusan National University, Busan, Republic of Korea.

Hepatitis B virus (HBV) encoding the HBV x protein (HBx) is a known causative agent of hepatocellular carcinoma (HCC). Its pathogenic activities in HCC include interference with several signaling pathways associated with cell proliferation and apoptosis. Mutant C-terminal-truncated HBx isoforms are frequently found in human HCC and have been shown to enhance proliferation and invasiveness leading to HCC malignancy. Read More

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April 2019
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Recent Advances in Organoid Culture for Insulin Production and Diabetes Therapy: Methods and Challenges.

BMB Rep 2019 Apr 3. Epub 2019 Apr 3.

Department of Stem Cell & Regenerative Biotechnology, Konkuk University, Gwangjin-gu, Seoul 05029, Korea.

Breakthroughs in stem cell technology have contributed to disease modeling and drug screening via organoid technology. Organoid are defined as three-dimensional cellular aggregations derived from adult tissues or stem cells. They recapitulate the intricate pattern and functionality of the original tissue. Read More

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April 2019
1 Read

Effects of α-lipoic acid on LPS-induced neuroinflammation and NLRP3 inflammasome activation through the regulation of BV-2 microglial cells activation.

BMB Rep 2019 Apr 3. Epub 2019 Apr 3.

Department of Biomedical Laboratory Science, Konyang University, Daejeon, Korea.

Microglial cells are known as the main immune cells in the central nervous system, both regulating its immune response and maintaining its homeostasis. Furthermore, the antioxidant α-lipoic acid (LA) is a recognized therapeutic drug for diabetes because it can easily invade the blood-brain barrier. This study investigated the effect of α-LA on the inflammatory response in lipopolysaccharide (LPS)-treated BV-2 microglial cells. Read More

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CpG-DNA induces bacteria-reactive IgM enhancing phagocytic activity against Staphylococcus aureus infection.

BMB Rep 2019 Apr 3. Epub 2019 Apr 3.

Department of Microbiology, College of Medicine, Hallym University, Chuncheon 24252, Republic of Korea; Center for Medical Science Research, College of Medicine, Hallym University, Chuncheon 24252, Republic of Korea.

CpG-DNA triggers the proliferation and differentiation of B cells which results in the increased production of antibodies. The presence of bacteria-reactive IgM in normal serum was reported; however, the relevance of CpG-DNA with the production of bacteria-reactive IgM has not been investigated. Here, we proved the function of CpG-DNA for the production of bacteria-reactive IgM. Read More

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April 2019
1 Read

Ahnak-knockout mice show susceptibility to Bartonella henselae infection because of CD4+ T cell inactivation and decreased cytokine secretion.

BMB Rep 2019 Apr 3. Epub 2019 Apr 3.

Laboratory of Developmental Biology and Genomics, BK21 Plus Program for Advanced Veterinary Science, Research Institute for Veterinary Science, College of Veterinary Medicine, and Korea Mouse Phenotyping Center, Seoul National University, Seoul 08826, Republic of Korea; Interdiscplinary Program for Bioinformatics, Seoul National University, Seoul 08826, Republic of Korea.

The present study evaluated the role of AHNAK in Bartonella henselae infection. Mice were intraperitoneally inoculated with 2 × 108 colony-forming units of B. henselae Houston-1 on day 0 and subsequently on day 10. Read More

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Insufficient radiofrequency ablation-induced autophagy contributes to the rapid progression of residual hepatocellular carcinoma through the HIF-1α/BNIP3 signaling pathway.

BMB Rep 2019 Apr 3. Epub 2019 Apr 3.

Department of Hepatobiliary Surgery, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing, China.

Currently speaking, it is noted that radiofrequency ablation (RFA) has been the most widely used treatment for hepatocellular carcinoma (HCC) occurring in patients. However, accumulating evidence has demonstrated that the incidence of insufficient RFA (IRFA) may result in the identified rapid progression of residual HCC in the patient, which can greatly hinder the effectiveness and patient reported benefits of utilizing this technique. Although many efforts have been proposed, the underlying mechanisms triggering the rapid progression of residual HCC after IRFA have not yet been fully clarified through current research literature reviews. Read More

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April 2019
1 Read

Elimination of Double-Strand Break End Resection Switches Recombination to the Non-homologous End Joining Pathway During Meiosis in Saccharomyces cerevisiae.

BMB Rep 2019 Apr 3. Epub 2019 Apr 3.

Department of Life Science, Chung-Ang University, Seoul 06974, Korea.

During meiosis, programmed double-strand breaks (DSBs) are repaired via recombination pathways that are required for faithful chromosomal segregation and genetic diversity. In meiotic progression, the non-homologous end joining (NHEJ) pathway is suppressed and instead meiotic recombination initiated by nucleolytic resection of DSB ends is the major pathway employed. This requires diverse recombinase proteins and regulatory factors involved in the formation of crossovers (COs) and non-crossovers (NCOs). Read More

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TP53I11 Suppresses Epithelial-mesenchymal Transition and Metastasis of Breast Cancer Cells.

BMB Rep 2019 Apr 3. Epub 2019 Apr 3.

CAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123, China; University of Science and Technology of China, Anhui 230026, China.

Epithelial-mesenchymal transition (EMT) is widely-considered to be a modulating factor of anoikis and cancer metastasis. We found that, in MDA-MB-231 cells, TP53I11 (tumor protein P53 inducible protein 11) suppressed EMT and migration in vitro, and inhibited metastasis in vivo. Our findings showed that hypoxic treatment upregulated the expression of HIF1α, but reduced TP53I11 protein levels and TP53I11 overexpression reduced HIF1α expression under normal culture and hypoxicconditions, and in xenografts of MDA-MB-231 cells. Read More

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MiR-371 Promotes Proliferation and Metastasis in Hepatocellular Carcinoma by Targeting PTEN.

BMB Rep 2019 Apr 3. Epub 2019 Apr 3.

Eastern Hepatobiliary Surgery Hospital (EHBH), Second Military Medical University, No 225, Changhai Road, Yangpu District, Shanghai City 200438, China.

Hepatocellular carcinoma (HCC) is the leading cause of cancer-related mortality worldwide. MiR-371 has recently emerged as an important regulator in tumorigenesis, and may serve as a biomarker for malignant tumors. We transfected miR-371 or its inhibitor in two human HCC cell lines, then used 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, soft agar colony formation, and transwell migration assays to evaluate the effects on cell proliferation, migration, and invasion. Read More

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April 2019
2 Reads

Erratum to: MiR-363 inhibits cisplatin chemoresistance of epithelial ovarian cancer by regulating snail-induced epithelial-mesenchymal transition.

BMB Rep 2019 03;52(3):226

The Institute of Medical Science Research, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P. R., China.

The BMB Reports would like to correct in the Supplementary Figure 1 of BMB Rep. 51(9): 456-461 titled "MiR-363 inhibits cisplatin chemoresistance of epithelial ovarian cancer by regulating snail-induced epithelial-mesenchymal transition." Read More

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Interleukin-2/antibody complex expanding Foxp3+ regulatory T cells exacerbates Th2-mediated allergic airway inflammation.

BMB Rep 2019 Mar 19. Epub 2019 Mar 19.

Academy of Immunology and Microbiology, Institute for Basic Science (IBS), Pohang, 37673, Republic of Korea; Department of Integrative Biosciences and Biotechnology. Pohang University of Science and Technology (POSTECH), Pohang, 37673, Republic of Korea.

Foxp3+ regulatory CD4+ T (Treg) cells play an essential role in preventing overt immune responses against self and innocuous foreign antigens. Selective expansion of endogenous Treg cells in response to the administration of interleukin (IL)-2/antibody complex, such as the IL-2/JES6-1 complex (IL-2C) in mice, is considered an attractive therapeutic approach to various immune disorders. Here, we investigated the therapeutic potential of IL-2C in allergic airway inflammation models. Read More

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Biological roles and an evolutionary sketch of the GRF-GIF transcriptional complex in plants.

Authors:
Jeong Hoe Kim

BMB Rep 2019 Mar 19. Epub 2019 Mar 19.

Department of Biology, School of Biological Sciences, Kyungpook National University, Daegu 41566, Korea.

GROWTH-REGULATING FACTORs (GRFs) are sequence-specific DNA-binding transcription factors that regulate various aspects of plant growth and development. GRF proteins interact with a transcription cofactor, GRF-INTERACTING FACTOR (GIF), to form a functional transcriptional complex. For its activities, the GRF-GIF duo requires the SWITCH2/SUCROSE NONFERMENTING2 chromatin remodeling complex. Read More

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Links between accelerated replicative cellular senescence and down-regulation of SPHK1 transcription.

BMB Rep 2019 Mar;52(3):220-225

Departments of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, Korea.

We have identified a mechanism to diminish the proliferative capacity of cells during cell expansion using human adiposederived stromal cells (hAD-SCs) as a model of replicative senescence. hAD-SCs of high-passage numbers exhibited a reduced proliferative capacity with accelerated cellular senescence. Levels of key bioactive sphingolipids were significantly increased in these senescent hAD-SCs. Read More

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March 2019
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N-terminal formylmethionine as a novel initiator and N-degron of eukaryotic proteins.

Authors:
Jeong-Mok Kim

BMB Rep 2019 Mar;52(3):163-164

Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 04763; Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Korea.

The ribosomal synthesis of proteins in the eukaryotic cytosol has always been thought to start from the unformylated N-terminal (Nt) methionine (Met). In contrast, in virtually all nascent proteins in bacteria and eukaryotic organelles, such as mitochondria and chloroplasts, Nt-formyl-methionine (fMet) is the first building block of ribosomal synthesis. Through extensive approaches, including mass spectrometric analyses of the N-termini of proteins and molecular genetic techniques with an affinity-purified antibody for Nt-formylation, we investigated whether Nt-formylated proteins could also be produced and have their own metabolic fate in the cytosol of a eukaryote, such as yeast Saccharomyces cerevisiae. Read More

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Deubiquitinating enzymes as cancer biomarkers: new therapeutic opportunities?

BMB Rep 2019 Mar;52(3):181-189

Graduate School of Biomedical Science and Engineering, Department of Biomedical Science, Hanyang University, Seoul 04763; College of Medicine, Hanyang University, Seoul 04763, Korea.

Cancer remains a life-threatening disease and accounts for the major mortality rates worldwide. The practice of using biomarkers for early detection, staging, and customized therapy may increase cancer patients' survival. Deubiquitinating enzymes (DUBs) are a family of proteases that remove ubiquitin tags from proteins of interest undergoing proteasomal degradation. Read More

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March 2019
5 Reads
2.595 Impact Factor

Epigenetic aspects of telomeric chromatin in Arabidopsis thaliana.

BMB Rep 2019 Mar;52(3):175-180

Department of Systems Biology, Yonsei University, Seoul 03722, Korea.

Telomeres are nucleoprotein complexes at the physical ends of linear eukaryotic chromosomes. They protect the chromosome ends from various external attacks to avoid the loss of genetic information. Telomeres are maintained by cellular activities associated with telomerase and telomerebinding proteins. Read More

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Acid sphingomyelinase-mediated blood-brain barrier disruption in aging.

BMB Rep 2019 Feb;52(2):111-112

KNU Alzheimer's disease Research Institute, Kyungpook National University, Daegu 41566; Department of Physiology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu 41944; Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu 41944, Korea.

Although many studies have reported that the breakdown of the blood-brain barrier (BBB) represents one of the major pathological changes in aging, the mechanism underlying this process remains relatively unexplored. In this study, we described that acid sphingomyelinase (ASM) derived from endothelial cells plays a critical role in BBB disruption in aging. ASM levels were elevated in the brain endothelium and plasma of aged humans and mice, resulting in BBB leakage through an increase in caveolae-mediated transcytosis. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443326PMC
February 2019
4 Reads

The coordinated regulation of mitochondrial structure and function by Drp1 for mitochondrial quality surveillance.

BMB Rep 2019 Feb;52(2):109-110

Department of Anatomy, Korea University College of Medicine, Brain Korea 21 Plus, Seoul 02841, Korea.

Mitochondrial morphology is known to be continuously changing via fusion and fission, but it is unclear what the biological importance of this energy-consuming process is and how it develops. Several data have suggested that mitochondrial fission executed by Drp1 is necessary to select out a damaged spot from the interconnected mitochondrial network, but the precise mechanism for the recognition and isolation of a damaged sub-mitochondrial region during mitochondrial fission is yet unclear. Recently, Cho et al. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443321PMC
February 2019

PRR11 and SKA2 gene pair is overexpressed and regulated by p53 in breast cancer.

BMB Rep 2019 Feb;52(2):157-162

Department of Biochemistry and Molecular Biology, Chongqing Medical University, Chongqing 400016, China.

Our previous study found that two novel cancer-related genes, PRR11 and SKA2, constituted a classic gene pair that was regulated by p53 and NF-Y in lung cancer. However, their role and regulatory mechanism in breast cancer remain elusive. In this study, we found that the expression levels of PRR11 and SKA2 were upregulated and have a negative prognotic value in breast cancer. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443325PMC
February 2019

NOD2 signaling pathway is involved in fibronectin fragment-induced pro-catabolic factor expressions in human articular chondrocytes.

BMB Rep 2019 Feb 14. Epub 2019 Feb 14.

Division of Rheumatology, Department of Internal Medicine, Hallym University Sacred Heart Hospital, Kyunggi, 14068, Korea; Institute for Skeletal Aging, Hallym University, Chunchon, 24251, Korea.

The nucleotide-binding and oligomerization domain (NOD) is an innate pattern recognition receptor that recognizes pathogen- and damage-associated molecular patterns. The 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) is a matrix degradation product found in the synovial fluids of patients with osteoarthritis (OA). We investigated whether NOD2 was involved in 29-kDa FN-f-induced pro-catabolic gene expression in human chondrocytes. Read More

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February 2019
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Mycoplasma exploits mammalian tunneling nanotubes for cell-to-cell dissemination.

BMB Rep 2019 Jan 24. Epub 2019 Jan 24.

Tunneling Nanotube Research Center, Korea University, Seoul 02841; Division of Life Sciences, Korea University, Seoul 02841, Republic of Korea.

Using tunneling nanotubes (TNTs), various pathological molecules and viruses disseminate to adjacent cells intercellularly. Here, we show that the intracellular invasion of Mycoplasma hyorhinis induces the formation of actin- and tubulin-based TNTs in various mammalian cell lines. M. Read More

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January 2019

Proteolytic cleavages of MET: the divide-and-conquer strategy of a receptor tyrosine kinase.

BMB Rep 2019 Jan 23. Epub 2019 Jan 23.

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Target Therapies, F-59000 Lille, France.

Membrane-anchored full-length MET stimulated by its ligand HGF/SF induces various biological responses, including survival, growth, and invasion. This panel of responses, referred to invasive growth, is required for embryogenesis and tissue regeneration in the adult. In contrast, MET deregulation is associated with tumorigenesis in many kinds of cancer. Read More

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January 2019

Regulation of IL-6 signaling by miR-125a and let-7e in endothelial cells controls vasculogenic mimicry formation of breast cancer cells.

BMB Rep 2019 Mar;52(3):214-219

Research Institute for Women's Health, Sookmyung Women's University, Seoul 04310, Korea.

The role of tumor-proximal factors in tumor plasticity during chemoresistance and metastasis following chemotherapy is well studied. However, the role of endothelial cell (EC) derived paracrine factors in tumor plasticity, their effect on chemotherapeutic outcome, and the mechanism by which these paracrine factors modulate the tumor microenvironment are not well understood. In this study, we report a novel mechanism by which endothelial miR-125a and let-7e-mediated regulation of interleukin-6 (IL-6) signaling can manipulate vasculogenic mimicry (VM) formation of MDA-MB-231 breast cancer cells. Read More

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March 2019
1 Read

JNK activation induced by ribotoxic stress is initiated from 80S monosomes but not polysomes.

BMB Rep 2019 Jan 23. Epub 2019 Jan 23.

Laboratory of Biochemistry, Division of Life Sciences, Korea University, Seoul 02841, Republic of Korea; HAEL Lab, TechnoComplex Building, Korea University, Seoul 02841, Republic of Korea.

Translation is a costly, but inevitable, cell maintenance process. To reduce unnecessary ATP consumption in cells, a fine-tuning mechanism is needed for both ribosome biogenesis and translation. Previous studies have suggested that the ribosome functions as a hub for many cellular signals such as ribotoxic stress response, mammalian target of rapamycin (mTOR), and ribosomal S6 kinase (RSK) signaling. Read More

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January 2019

Deciphering the molecular mechanisms underlying the plasma membrane targeting of PRMT8.

BMB Rep 2019 Jan 23. Epub 2019 Jan 23.

Department of Ecological Science, College of Ecology and Environment, Kyungpook National University, 2559, Gyeongsang-daero, Sangju-si, Gyeongsangbuk-do 37224, Republic of Korea.

Arginine methylation plays crucial roles in many cellular functions including signal transduction, RNA transcription, and regulation of gene expression. Protein arginine methyltransferase 8 (PRMT8), a unique brain-specific protein, is localized to the plasma membrane. However, the detailed molecular mechanisms underlying PRMT8 plasma membrane targeting remain unclear. Read More

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January 2019

A chemical conjugate between HER2-targeting antibody fragment and Pseudomonas exotoxin A fragment demonstrates cytotoxic effects on HER2-expressing breast cancer cells.

BMB Rep 2019 Jan 23. Epub 2019 Jan 23.

Department of Physiology, Bio-Medical Institute of Technology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea.

Conventionally, immunotoxins have been produced as a single polypeptide from fused genes of an antibody fragment and a toxin. In this study, we adopted a unique approach of chemical conjugation of a toxin protein and an antibody fragment. The two genes were separately expressed in Escherichia coli and purified to high levels of purity. Read More

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January 2019

Endothelial-specific deletion of Ets-1 attenuates Angiotensin II-induced cardiac fibrosis via suppression of endothelial-to-mesenchymal transition.

BMB Rep 2019 Jan 23. Epub 2019 Jan 23.

State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension, Ruijin Hospital and Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Cardiac fibrosis is a common feature in chronic hypertension patients with advanced heart failure, and endothelial-to-mesenchymal transition (EndMT) is known to promote Angiotensin II (Ang II)-mediated cardiac fibrosis. Previous studies have suggested a potential role for the transcription factor, ETS-1, in Ang II-mediated cardiac remodeling, however the mechanism are not well defined. In this study, we found that mice with endothelial Ets-1 deletion showed reduced cardiac fibrosis and hypertrophy following Ang II infusion. Read More

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January 2019
2 Reads

2-(trimethylammonium)ethyl (R)-3-methoxy-3-oxo-2-stearamidopropyl phosphate enhances thrombopoietin-induced megakaryocytic differentiation and plateletogenesis.

BMB Rep 2019 Jan 23. Epub 2019 Jan 23.

Department of Life Science, Ewha Womans University, Seoul 03760 Korea.

We have previously reported the effects of 2-(trimethylammonium)ethyl (R)-3-methoxy-3-oxo-2-stearamidopropyl phosphate [(R)-TEMOSPho], a synthetic phospholipid, on megakaryocytic differentiation of myeloid leukemia cells. Here, we demonstrate that (R)-TEMOSPho enhances megakaryopoiesis and plateletogenesis from primary hematopoietic stem cells (HSCs) induced by thrombopoietin (TPO). Specifically, we demonstrate at sub-saturation levels of TPO, the addition of (R)-TEMOSPho enhances differentiation and maturation of megakaryocytes (MKs) from murine HSCs derived from fetal liver. Read More

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January 2019

Surface expression of TTYH2 is attenuated by direct interaction with β-COP.

BMB Rep 2019 Jan 23. Epub 2019 Jan 23.

School of Biosystem and Biomedical Science, College of Health Science, Korea University, Seoul 136-703, Republic of Korea.

TTYH2 is a calcium-activated, inwardly rectifying anion channel that has been shown to be related to renal cancer and colon cancer. Based on the topological prediction, TTYH2 protein has five transmembrane domains with the extracellular N-terminus and the cytoplasmic C-terminus. In the present study, we identified a vesicle transport protein, β-COP, as a novel specific binding partner of TTYH2 by yeast two-hybrid screening using a human brain cDNA library with the C-terminal region of TTYH2 (TTYH2-C) as a bait. Read More

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January 2019
1 Read

Interleukin-32: Frenemy in cancer?

Authors:
Sora Han Young Yang

BMB Rep 2019 Mar;52(3):165-174

Department of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.

Interleukin-32 (IL-32) was originally identified in natural killer (NK) cells activated by IL-2 in 1992. Thus, it was named NK cell transcript 4 (NK4) because of its unknown function at that time. The function of IL-32 has been elucidated over the last decade. Read More

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Regulation of post-translational modification in breast cancer treatment.

Authors:
Kyung-Sun Heo

BMB Rep 2019 Feb;52(2):113-118

College of Pharmacy and Institute of Drug Research and Development, Chungnam National University, Daejeon 34134, Korea.

The small ubiquitin-related modification molecule (SUMO), one of the post-translational modification molecules, is involved in a variety of cellular functions where it regulates protein activity and stability, transcription, and cell cycling. Modulation of protein SUMOylation or deSUMOylation modification has been associated with regulation of carcinogenesis in breast cancer. In the dynamic processes of SUMOylation and deSUMOylation in a variety of cancers, SUMO proteases (SENPs), reverse SUMOylation by isopeptidase activity and SENPs are mostly elevated, and are related to poor patient prognosis. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443327PMC
February 2019

E3 ubiquitin ligases and deubiquitinases as modulators of TRAIL-mediated extrinsic apoptotic signaling pathway.

BMB Rep 2019 Feb;52(2):119-126

Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Korea.

The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) initiates the extrinsic apoptotic pathway through formation of the death-inducing signaling complex (DISC), followed by activation of effector caspases. TRAIL receptors are composed of death receptors (DR4 and DR5), decoy receptors (DcR1 and DcR2), and osteoprotegerin. Among them, only DRs activate apoptotic signaling by TRAIL. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443324PMC
February 2019
1 Read

Cellular senescence, aging, and age-related disease: Special issue of BMB Reports in 2019.

Authors:
Jae-Seon Lee

BMB Rep 2019 Jan;52(1):1-2

Hypoxia-related Disease Research Center and Department of Molecular Biology, College of Medicine, Inha University, Incheon 22212, Korea.

Cellular senescence is a state of permanent cell cycle arrest which exhibits large and flattened morphological characteristics. Cellular senescence might evolve to a beneficial process to suppress the accumulation of severely damaged cells. However, senescent cells are considered as the cause of age-related pathologies and diseases. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386232PMC
January 2019

Endothelial dysfunction induces atherosclerosis: increased aggrecan expression promotes apoptosis in vascular smooth muscle cells.

BMB Rep 2019 Feb;52(2):145-150

Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine; Department of Biochemistry and Molecular Biology, Asan Medical Center, University of Ulsan College of Medicine; Stem Cell Immunomodulation Research Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.

Endothelial dysfunction-induced lipid retention is an early feature of atherosclerotic lesion formation. Apoptosis of vascular smooth muscle cells (VSMCs) is one of the major modulating factors of atherogenesis, which accelerates atherosclerosis progression by causing plaque destabilization and rupture. However, the mechanism underlying VSMC apoptosis mediated by endothelial dysfunction in relation to atherosclerosis remains elusive. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443320PMC
February 2019

MicroRNA-152-5p inhibits proliferation and migration and promotes apoptosis by regulating expression of Smad3 in human keloid fibroblasts.

BMB Rep 2019 Mar;52(3):202-207

Department of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.

Keloids are the most common pathological form of trauma healing, with features that seriously affect appearance and body function, are difficult to treat and have a high recurrence rate. Emerging evidence suggests that miRNAs are involved in a variety of pathological processes and play an important role in the process of fibrosis. In this study, we investigated the function and regulatory network of miR-152-5p in keloids. Read More

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Downregulation of FoxM1 sensitizes nasopharyngeal carcinoma cells to cisplatin via inhibition of MRN-ATM-mediated DNA repair.

BMB Rep 2019 Mar;52(3):208-213

Department of Otolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 40016, China.

Chemoresistance is the primary obstacle in the treatment of locally advanced and metastatic nasopharyngeal carcinoma (NPC). Recent evidence suggests that the transcription factor forkhead box M1 (FoxM1) is involved in chemoresistance. Our group previously confirmed that FoxM1 is overexpressed in NPC. Read More

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March 2019
9 Reads

High expression of RAD51 promotes DNA damage repair and survival in KRAS-mutant lung cancer cells.

BMB Rep 2019 Feb;52(2):151-156

Department of Oncology, Beijing Daxing District People's Hospital, Capital Medical University, Beijing 102600, China.

RAD51 recombinase plays a critical role in homologous recombination and DNA damage repair. Here we showed that expression of RAD51 is frequently upregulated in lung cancer tumors compared with normal tissues and is associated with poor survival (hazard ratio (HR) = 2, P = 0.0009). Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443323PMC
February 2019
1 Read
2.595 Impact Factor

HSP90 inhibitor, AUY922, debilitates intrinsic and acquired lapatinib-resistant HER2-positive gastric cancer cells.

BMB Rep 2018 Dec;51(12):660-665

Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.

Human epidermal growth factor receptor 2 (HER2) inhibitors, such as trastuzumab and lapatinib are used to treat HER2-positive breast and gastric cancers. However, as with other targeted therapies, intrinsic or acquired resistance to HER2 inhibitors presents unresolved therapeutic problems for HER2-positive gastric cancer. The present study describes investigations with AUY922, a heat shock protein 90 (HSP90) inhibitor, in primary lapatinib-resistant (ESO26 and OE33) and lapatinib-sensitive gastric cancer cells (OE19, N87, and SNU-216) harboring HER2 amplification/over-expression. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330940PMC
December 2018
2 Reads

Modulation of senoinflammation by calorie restriction based on biochemical and Omics big data analysis.

BMB Rep 2019 Jan;52(1):56-63

Department of Pharmacy, College of Pharmacy, Pusan National University, Busan 46241, Korea.

Aging is a complex and progressive process characterized by physiological and functional decline with time that increases susceptibility to diseases. Aged-related functional change is accompanied by a low-grade, unresolved chronic inflammation as a major underlying mechanism. In order to explain aging in the context of chronic inflammation, a new integrative concept on age-related chronic inflammation is necessary that encompasses much broader and wider characteristics of cells, tissues, organs, systems, and interactions between immune and non-immune cells, metabolic and non-metabolic organs. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386225PMC
January 2019
1 Read
2.595 Impact Factor

Mitochondria: multifaceted regulators of aging.

BMB Rep 2019 Jan;52(1):13-23

Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089; USC Norris Comprehensive Cancer Center, Los Angeles, CA 90089, USA; Biomedical Science, Graduate School, Ajou University, Suwon 16499, Korea.

Aging is accompanied by a time-dependent progressive deterioration of multiple factors of the cellular system. The past several decades have witnessed major leaps in our understanding of the biological mechanisms of aging using dietary, genetic, pharmacological, and physical interventions. Metabolic processes, including nutrient sensing pathways and mitochondrial function, have emerged as prominent regulators of aging. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386233PMC
January 2019
17 Reads

Growth signaling and longevity in mouse models.

BMB Rep 2019 Jan;52(1):70-85

Institute of Animal Molecular Biotechnology, Korea University, Seoul 02841; Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02481, Korea.

Reduction of insulin/insulin-like growth factor 1 (IGF1) signaling (IIS) extends the lifespan of various species. So far, several longevity mouse models have been developed containing mutations related to growth signaling deficiency by targeting growth hormone (GH), IGF1, IGF1 receptor, insulin receptor, and insulin receptor substrate. In addition, p70 ribosomal protein S6 kinase 1 (S6K1) knockout leads to lifespan extension. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386229PMC
January 2019
3 Reads

Tat-ATOX1 inhibits inflammatory responses via regulation of MAPK and NF-κB pathways.

BMB Rep 2018 Dec;51(12):654-659

Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea.

Antioxidant 1 (ATOX1) protein has been reported to exhibit various protective functions, including antioxidant and chaperone. However, the effects of ATOX1 on the inflammatory response has not been fully elucidated. Thus, we prepared cell permeable Tat-ATOX1 and studied the effects on lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13- acetate (TPA)-induced inflammation. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330941PMC
December 2018
7 Reads
2.595 Impact Factor

SETDB1 regulates SMAD7 expression for breast cancer metastasis.

BMB Rep 2019 Feb;52(2):139-144

Korea Research Institute of Bioscience and Biotechnology, and Department of Functional Genomics, Korea University of Science and Technology, Daejeon 34141, Korea.

Breast cancer (BRC) is the most invasive cancer in women. Although the survival rate of BRC is gradually increasing due to improved screening systems, development of novel therapeutic targets for inhibition of BRC proliferation, metastasis and recurrence have been constantly needed. Thus, in this study, we identified overexpression of SETDB1 (SET Domain Bifurcated 1), a histone methyltransferase, in RNA-seq data of BRC derived from TCGA portal. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443319PMC
February 2019

SPINK1 promotes cell growth and metastasis of lung adenocarcinoma and acts as a novel prognostic biomarker.

BMB Rep 2018 Dec;51(12):648-653

Department of Cardio-Thoracic Surgery, Affiliated Zhoushan Hospital of Wenzhou Medical University, Zhoushan 316000, China.

Serine protease inhibitor Kazal type 1 (SPINK1) plays a role in protecting the pancreas against premature activation of trypsinogen and is involved in cancer progression. SPINK1 promoted LAC cells growth, migration, and invasion. Mechanistically, we found that SPINK1 promoted LAC cells migration and invasion via up-regulating matrix metalloproteinase 12 (MMP12). Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330943PMC
December 2018

Disease model organism for Parkinson Disease: Drosophila melanogaster.

BMB Rep 2018 Dec 14. Epub 2018 Dec 14.

Department of Bio and Fermentation Convergence Technology, Kookmin University, BK21 PLUS Project, Seoul 02707, Republic of Korea.

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by selective and progressive loss of dopaminergic neurons. Genetic and environmental risk factors are associated with this disease. The genetic factors are composed of approximately 20 genes, such as SNCA, parkin, PTEN-induced kinase1 (pink1), leucine-rich repeat kinase 2 (LRRK2), ATP13A2, MAPT, VPS35, and DJ-1, whereas the environmental factors consist of oxidative stress-induced toxins such as 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), rotenone, and paraquat. Read More

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December 2018

UBE2S promotes the proliferation and survival of human lung adenocarcinoma cells.

Authors:
Zhi Liu Lijun Xu

BMB Rep 2018 Dec;51(12):642-647

Department of Respiratory Medicine, The First Hospital of Jilin University, Changchun 130021, China.

Ubiquitin-conjugating enzyme E2S (UBE2S), a family of E2 protein in the ubiquitination process, is involved in development of various cancers. However, its role in lung adenocarcinoma, has not been well elucidated. In this report, we attempted to investigate expression and function of UBE2S in lung adenocarcinoma. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330942PMC
December 2018
11 Reads

Multi-level remodeling of transcriptional landscapes in aging and longevity.

BMB Rep 2019 Jan;52(1):86-108

Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089; USC Norris Comprehensive Cancer Center, Epigenetics and Gene Regulation, Los Angeles, CA 90089; USC Stem Cell Initiative, Los Angeles, CA 90089, USA.

In multi-cellular organisms, the control of gene expression is key not only for development, but also for adult cellular homeostasis, and gene expression has been observed to be deregulated with aging. In this review, we discuss the current knowledge on the transcriptional alterations that have been described to occur with age in metazoans. First, we discuss age-related transcriptional changes in protein-coding genes, the expected functional impact of such changes, and how known pro-longevity interventions impact these changes. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386224PMC
January 2019
2 Reads

Cellular senescence in cancer.

BMB Rep 2019 Jan;52(1):42-46

Department of Biochemistry and Molecular Biology, Ajou University School of Medicine, Suwon 16499, Korea.

Cellular senescence, a process of cell proliferation arrest in response to various stressors, has been considered to be important factor in age-related disease. Identification of senescent cells in tissues is limited and the role of senescent cells is poorly understood. Recently however, several studies showed the characterization of senescent cells in various pathologic conditions and the role of senescent cells in disease progression is becoming important. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386235PMC
January 2019

Cellular senescence: a promising strategy for cancer therapy.

BMB Rep 2019 Jan;52(1):35-41

Hypoxia-related Disease Research Center, and Department of Molecular Medicine, College of Medicine, Inha University, Incheon 22212, Korea.

Cellular senescence, a permanent state of cell cycle arrest, is believed to have originally evolved to limit the proliferation of old or damaged cells. However, it has been recently shown that cellular senescence is a physiological and pathological program contributing to embryogenesis, immune response, and wound repair, as well as aging and age-related diseases. Unlike replicative senescence associated with telomere attrition, premature senescence rapidly occurs in response to various intrinsic and extrinsic insults. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386234PMC
January 2019