• Journal of Life Science
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• v.25 no.2
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• pp.223-230
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• 2015

Regulator of calcineurin 1 (RCAN1) is an endogenous calcineurin inhibitor that plays an important role in the pathogenesis of diseases related to the calcineurin-NFATc1 signaling pathway. The RCAN1-4 isoform is subject to NFATc1-dependent regulation. During receptor activator of nuclear factor kappa-B ligand (RANKL)-stimulated osteoclastogenesis, the calcineurin-NFATc1 pathway is critical. Because there is little information available on the role of RCAN1 in osteoclast differentiation, this study investigated whether changes in RCAN1 expression are related to the calcineurin-NFATc1 pathway and osteoclast differentiation. Mouse bone marrow monocytes (BMMs) were treated with 50 ng/ml of RANKL and M-CSF. Expression levels of NFATc1, calcineurin, and RCAN1 isoforms were determined using RT-PCR and Western blotting. Osteoclast differentiation was examined using tartrate-resistent acid phosphatase (TRAP) staining. To evaluate the effect of RCAN1 overexpression on osteoclastogenesis, cells were transfected with a mouse RCAN1-4 cDNA plasmid. After RANKL stimulation of BMMs, expression of NFATc1 and RCAN1 was increased at the mRNA and protein level, while calcineurin expression was unchanged. When the RCAN1-4 gene construct was transfected, the expression of RCAN1 protein was not increased despite several-fold increases in RCAN1-4 mRNA expression. Regardless of RANKL stimulation, over-expression of RCAN1-4 tended to reduce NFATc1 expression and knock-down of RCAN1 increase it. While BMMs transfected with the RCAN1-4 vector were differentiated into distinct osteoclasts, their phenotypes did not vary from those of mock controls. These results suggest that RCAN1 has a limited effect on the calcineurin-NFATc1 pathway during RANKL-stimulated osteoclast differentiation.

• 한국생물공학회:학술대회논문집
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• 2005.10a
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• pp.293-294
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• 2005

• Journal of the korean Society of Automotive Engineers
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• v.16 no.4
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• pp.51-61
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• 1994

기관의 출력성능은 기관으로 공급되는 연료공기의 혼합기량에 따라서 크게 달라진다. 이것은 기관의 출력성능은 기관으로 공급되는 흡기 용량에 따라서 변화하기 때문이다. 고출력을 얻기 위하여는 동일한 조건의 경우 흡기량을 증가시켜 기관 실린더 내에서 많은 연소 열에너지를 생성하는 것이 필요하다. 이러한 관점에서 기관의 체적 효율(volumetric efficiency)을 증가시킬 목적으로 여러가지 흡기 계통의 개서을 도모하고 있으나 흡기 용량을 증가시키는 방법의 하나는 과급기(supercharger)를 이용하는 과급 방식이다. 이와같은 과급방식은 기관의 출력성능의 향상을 가져오지만 기관 내부의 노크(knock), 연소 압력 및 열부하의 증가, 연비 문제등에 관한 여러가지 문제점이 제기되고 있다. 여기서는 과급에 적용되는 과급기의 종류와 과급 성능 특성 등에 대하여 살펴보고 과급기관의 성능에 대하여 다루기로 한다.

• Journal of the korean Society of Automotive Engineers
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• v.12 no.1
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• pp.6-9
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• 1990

본 고에서는 녹킹현상과 녹킹 발생의 결과, 그리고 녹킹과 연료와의 관계등에 대해 개략적으로 설명하려 한다. 녹킹 발생 유무는 흡입공기상태, 스로틀 열림정도, 연소실 형상, 스파크 점화시기, 화염 전파속도 및 연료의 자연 발화 특성에 관계되며 화염 전파속도와 end-gas에 있는 연로의 반응속도와의 경쟁이라 볼수 있다. 연료의 녹킹 발생에 대한 저항성을 나탄내는 척도가 옥탄가이며 옥탄가가 높을 수록 자연 발화하기 어려우므로 녹킹이 잘 일어나지 않는다.

• Journal of the Korea Safety Management & Science
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• v.9 no.2
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• pp.183-194
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• 2007

1. Through this experiment, we made certain that the best distinguished frequency area of the Hyundae Beta 2.0 engine's knocking is 6.8khz. 2. Through the experiment, we checked the output power voltage condition of the logging output with the generation of a engine knocking. And wechecked up that it generated maximumly up to 11.4 V which depends on the degree of the streng.

• International Journal of High-Rise Buildings
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• v.11 no.1
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• pp.41-50
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• 2022

The Spiral, a supertall tower at the Hudson Yards Zoning District of NYC is an new iconic commercial office tower. The spiraling terraces throughout the height of the building creates unique outdoor spaces at each level for its occupants while introduces structural challenges unlike common office towers. Innovative structural solutions and an integrated connection design and steel detailing delivery process proved to be a key factor in the success of the project.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5865-5869
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• 2012

RHOXF1 has been shown to be expressed in embryonic stem cells, adult germline stem cells and some cancer lines. It has been proposed as a candidate gene to encode transcription factors regulating downstream genes in the human testis with antiapoptotic effects. Its expression in cancer cell lines has implied a similar role in the process of tumorigenesis. The human breast cancer cell lines MDA-MB-231 and MCF-7 were cultured in DMEM medium and transfected with a pGFP-V-RS plasmid bearing an RHOXF1 specific shRNA. Quantitative real-time RT-PCR was performed for RHOXF1, CASP8, BCL2 and HPRT genes. Decreased RHOXF1 expression was confirmed in cells after transfection. shRNA knock down of RHOXF1 resulted in significantly decreased BCL2 expression in both cell lines but no change in CASP8 expression. shRNA targeting RHOXF1 was shown to specifically mediate RHOXF1 gene silencing, so RHOXF1 can mediate transcriptional activation of the BCL2 in cancers and may render tumor cells resistant to apoptotic cell death induced by anticancer therapy. shRNA mediated knock down of RHOXF1 can be effective in induction of apoptotic pathway in cancer cells via BCL2 downregulation, so it can have potential therapeutic utility for human breast cancer.

• BMB Reports
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• v.45 no.8
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• pp.470-475
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• 2012

Protein arginine methyltransferase 1 (PRMT1), a type-I arginine methyltransferase, has been implicated in diverse cellular events. We have focused on the role of PRMT1 in gliomagenesis. In this study, we showed that PRMT1 expression was up-regulated in glioma tissues and cell lines compared with normal brain tissues. The knock-down of PRMT1 resulted in an arrest in the G1-S phase of the cell cycle, proliferation inhibition and apoptosis induction in four glioma cell lines (T98G, U87MG, U251, and A172). Moreover, an in vivo study confirmed that the tumor growth in nude mouse xenografts was significantly decreased in the RNAi-PRMT1 group. Additionally, we found that the level of the asymmetric dimethylated modification of H4R3, a substrate of PRMT1, was higher in glioma cells than in normal brain tissues and decreased after PRMT1 knock-down. Our data suggest a potential role for PRMT1 as a novel biomarker of and therapeutic target in gliomas.

• Research in Plant Disease
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• v.16 no.3
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• pp.312-315
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• 2010

Pectobacterium carotovorum subsp. carotovorum (Pcc) causes soft rot disease in various plants. Although many studies about Pcc have been going on, little is known yet about the defense genes from plants. To identify defense associated genes in response to Pcc, we screened about 20 thousand Arabidopsis T-DNA knock out lines by inoculation with Pcc. We obtained a line (Atspt1) showing more susceptible symptom compared to WT (Col-0) on 1 day after the inoculation of Pcc on leaves of Arabidopsis with toothpicks. In this study, we optimized the system to select resistant and susceptible lines to Pcc from T-DNA inserted pool of Arabidopsis and expect the system and Atspt1 might be used for molecular breeding to produce resistant vegetables against Pcc.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.1
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• pp.65-71
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• 2013

The transient receptor potential melastatin type 7 (TRPM7) channel is a widely expressed non-selective cation channel with fusion to the C-terminal alpha kinase domain and regarded as a key regulator of whole body $Mg^{2+}$ homeostasis in mammals. However, the roles of TRPM7 during osteoclastogenesis in RAW264.7 cells and bone marrow-derived monocyte/macrophage precursor cells (BMMs) are not clear. In the present study, we investigate the roles of TRPM7 in osteoclastogenesis using methods of small interfering RNA (siRNA), RT-PCR, patch-clamp, and calcium imaging. RANKL (receptor activator of NF-${\kappa}B$ ligand) stimulation did not affect the TRPM7 expression and TRPM7-mediated current was activated in HEK293, RAW264.7, and BMM cells by the regulation of $Mg^{2+}$. Knock-down of TRPM7 by siTRPM7 reduced intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) increases by 0 mM $[Mg^{2+}]_e$ in HEK293 cells and inhibited the generation of RANKL-induced $Ca^{2+}$ oscillations in RAW264.7 cells. Finally, knock-down of TRPM7 suppressed RANKL-mediated osteoclastogenesis such as activation and translocation of NFATc1, formation of multinucleated cells, and the bone resorptive activity, sequentially. These results suggest that TRPM7 plays an essential role in the RANKL-induced $[Ca^{2+}]_i$ oscillations that triggers the late stages of osteoclastogenesis.