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REFERENCE LINKING PLATFORM OF KOREA S&T JOURNALS
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Journal DOI :
Korean Society for Biochemistry and Molecular Biology
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Volume & Issues
Volume 47, Issue 12 - Dec 2014
Volume 47, Issue 11 - Nov 2014
Volume 47, Issue 10 - Oct 2014
Volume 47, Issue 9 - Sep 2014
Volume 47, Issue 8 - Aug 2014
Volume 47, Issue 7 - Jul 2014
Volume 47, Issue 6 - Jun 2014
Volume 47, Issue 5 - May 2014
Volume 47, Issue 4 - Apr 2014
Volume 47, Issue 3 - Mar 2014
Volume 47, Issue 2 - Feb 2014
Volume 47, Issue 1 - Jan 2014
Selecting the target year
Ginsberg, Mark H. ;
BMB Reports , volume 47, issue 12, 2014, Pages 655~659
DOI : 10.5483/BMBRep.2014.47.12.241
Integrin-mediated cell adhesion is important for development, immune responses, hemostasis and wound healing. Integrins also function as signal transducing receptors that can control intracellular pathways that regulate cell survival, proliferation, and cell fate. Conversely, cells can modulate the affinity of integrins for their ligands a process operationally defined as integrin activation. Analysis of activation of integrins has now provided a detailed molecular understanding of this unique form of "inside-out" signal transduction and revealed new paradigms of how transmembrane domains (TMD) can transmit long range allosteric changes in transmembrane proteins. Here, we will review how talin and mediates integrin activation and how the integrin TMD can transmit these inside out signals.
Stathmin 1 in normal and malignant hematopoiesis
Machado-Neto, Joao Agostinho ; Saad, Sara Teresinha Olalla ; Traina, Fabiola ;
BMB Reports , volume 47, issue 12, 2014, Pages 660~665
DOI : 10.5483/BMBRep.2014.47.12.020
Stathmin 1 is a microtubule destabilizer that plays an important role in cell cycle progression, segregation of chromosomes, clonogenicity, cell motility and survival. Stathmin 1 overexpression has been reported in malignant hematopoietic cells and Stathmin 1 inhibition reduces the highly proliferative potential of leukemia cell lines. However, during the differentiation of primary hematopoietic cells, Stathmin 1 expression decreases in parallel to decreases in the proliferative potential of early hematopoietic progenitors. The scope of the present review is to survey the current knowledge and highlight future perspectives for Stathmin 1 in normal and malignant hematopoiesis, with regard to the expression, function and clinical implications of this protein.
Role of Wnt signaling in fracture healing
Xu, Huiyun ; Duan, Jing ; Ning, Dandan ; Li, Jingbao ; Liu, Ruofei ; Yang, Ruixin ; Jiang, Jean X. ; Shang, Peng ;
BMB Reports , volume 47, issue 12, 2014, Pages 666~672
DOI : 10.5483/BMBRep.2014.47.12.193
The Wnt signaling pathway is well known to play major roles in skeletal development and homeostasis. In certain aspects, fracture repair mimics the process of bone embryonic development. Thus, the importance of Wnt signaling in fracture healing has become more apparent in recent years. Here, we summarize recent research progress in the area, which may be conducive to the development of Wnt-based therapeutic strategies for bone repair.
PV.1 induced by FGF-Xbra functions as a repressor of neurogenesis in Xenopus embryos
Yoon, Jaeho ; Kim, Jung-Ho ; Lee, Sung-Young ; Kim, SungChan ; Park, Jae-Bong ; Lee, Jae-Yong ; Kim, Jaebong ;
BMB Reports , volume 47, issue 12, 2014, Pages 673~678
DOI : 10.5483/BMBRep.2014.47.12.290
During Xenopus early development, FGF signaling is involved in mesoderm formation and neurogenesis by modulating various signaling cascades. FGF-MAPK signaling induces Xbra expression, which maintains mesodermal fate through an autocatalytic-loop. Interestingly, previous reports have demonstrated that basic FGF (bFGF) treatment alone does not induce neurogenesis in ectodermal explants, even though FGF signaling inhibits BMP signaling via phosphorylation in Smad1 linker region. In addition, the overexpression of dominantnegative Xbra induces neurogenesis in ectodermal explants. However, the detailed mechanism underlying these phenomena has not yet been clarified. In this work, we showed that bFGF-Xbra signaling increased the PV.1 expression. DN-Xbra was found to decrease PV.1 expression, and the co-injection of PV.1 with DN-Xbra reduced neurogenesis in ectodermal explants. Furthermore, the knockdown of PV.1 induced neurogenesis in bFGF-treated ectodermal explants. Taken together, our results demonstrate that FGF-Xbra signaling induces PV.1 expression and that PV.1 functions as a neural repressor in the FGF-treated ectoderm.
GM-CSF reduces expression of chondroitin sulfate proteoglycan (CSPG) core proteins in TGF-β-treated primary astrocytes
Choi, Jung-Kyoung ; Park, Sang-Yoon ; Kim, Kil Hwan ; Park, So Ra ; Lee, Seok-Geun ; Choi, Byung Hyune ;
BMB Reports , volume 47, issue 12, 2014, Pages 679~684
DOI : 10.5483/BMBRep.2014.47.12.018
GM-CSF plays a role in the nervous system, particularly in cases of injury. A therapeutic effect of GM-CSF has been reported in rat models of various central nervous system injuries. We previously showed that GM-CSF could enhance long-term recovery in a rat spinal cord injury model, inhibiting glial scar formation and increasing the integrity of axonal structure. Here, we investigated molecular the mechanism(s) by which GM-CSF suppressed glial scar formation in an in vitro system using primary astrocytes treated with TGF-
. GM-CSF repressed the expression of chondroitin sulfate proteoglycan (CSPG) core proteins in astrocytes treated with TGF-
. GM-CSF also inhibited the TGF-
-induced Rho-ROCK pathway, which is important in CSPG expression. Finally, the inhibitory effect of GM-CSF was blocked by a JAK inhibitor. These results may provide the basis for GM-CSF's effects in glial scar inhibition and ultimately for its therapeutic effect on neural cell injuries.
Constitutively active Ras negatively regulates Erk MAP kinase through induction of MAP kinase phosphatase 3 (MKP3) in NIH3T3 cells
Park, Young Jae ; Lee, Jong Min ; Shin, Soon Young ; Kim, Young Ho ;
BMB Reports , volume 47, issue 12, 2014, Pages 685~690
DOI : 10.5483/BMBRep.2014.47.12.017
The Ras/Raf/MEK/Erk signaling pathway is important for regulation of cell growth, proliferation, differentiation, survival, and apoptosis in response to a variety of extracellular stimuli. Lack of Erk MAPK activation is observed in several cancer cells despite active activation of Ras. However, little is known about the modulation of Erk1/2 activity by active Ras. Here, we show that overexpression of active H-Ras (H-RasG12R) in NIH3T3 fibroblasts impaired FGF2-induced Erk1/2 phosphorylation, as compared to wild-type cells. Northern blot analysis revealed that prolonged expression of active Ras increased MAP kinase phosphatase 3 (MKP3) mRNA expression, a negative regulator of Erk MAPK. Inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway abrogated active Ras-induced up-regulation of MKP3 expression, leading to the rescue of Erk1/2 phosphorylation. Our results demonstrated that the Ras/Raf/MEK/Erk signaling cascade is negatively regulated by the PI3K/Aktdependent transcriptional activation of the MKP3 gene.
Seahorse-derived peptide suppresses invasive migration of HT1080 fibrosarcoma cells by competing with intracellular α-enolase for plasminogen binding and inhibiting uPA-mediated activation of plasminogen
Kim, Yong-Tae ; Kim, Se-Kwon ; Jeon, You-Jin ; Park, Sun Joo ;
BMB Reports , volume 47, issue 12, 2014, Pages 691~696
DOI : 10.5483/BMBRep.2014.47.12.235
-Enolase is a glycolytic enzyme and a surface receptor for plasminogen.
-Enolase-bound plasminogen promotes tumor cell invasion and cancer metastasis by activating plasmin and consequently degrading the extracellular matrix degradation. Therefore,
-enolase and plasminogen are novel targets for cancer therapy. We found that the amino acid sequence of a peptide purified from enzymatic hydrolysates of seahorse has striking similarities to that of
-enolase. In this study, we report that this peptide competes with cellular
-enolase for plasminogen binding and suppresses urokinase plasminogen activator (uPA)-mediated activation of plasminogen, which results in decreased invasive migration of HT1080 fibrosarcoma cells. In addition, the peptide treatment decreased the expression levels of uPA compared to that of untreated controls. These results provide new insight into the mechanism by which the seahorse-derived peptide suppresses invasive properties of human cancer cells. Our findings suggest that this peptide could emerge as a potential therapeutic agent for cancer.
Celastrol inhibits gastric cancer growth by induction of apoptosis and autophagy
Lee, Hyun-Woo ; Jang, Kenny Seung Bin ; Choi, Hye Ji ; Jo, Ara ; Cheong, Jae-Ho ; Chun, Kyung-Hee ;
BMB Reports , volume 47, issue 12, 2014, Pages 697~702
DOI : 10.5483/BMBRep.2014.47.12.069
Recently, the interest in natural products for the treatment of cancer is increasing because they are the pre-screened candidates. In the present study, we demonstrate the therapeutic effect of celastrol, a triterpene extracted from the root bark of Chinese medicine on gastric cancer. The proliferation of AGS and YCC-2 cells were most sensitively decreased in six kinds of gastric cancer cell lines after the treatment with celastrol. Celastrol inhibited the cell migration and increased G1 arrest in cell-cycle populations in both cell lines. The treatment with celastrol significantly induced autophagy and apoptosis and increased the expression of autophagy and apoptosis-related proteins. We also found an increase in phosphorylated AMPK following a decrease in all phosphorylated forms of AKT, mTOR and S6K after the treatment with celastrol. Moreover, gastric tumor burdens were reduced in a dose-dependent manner by celastrol administration in a xenografted mice model. Taken together, celastrol distinctly inhibits the gastric cancer cell proliferation and induces autophagy and apoptosis.