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Wang Zengsheng,Li Yan,Kuang Xiaochuan,Guo Fang,Lang Tao,Mao Min,Zhang Xiaoyan,Yang Haiqing 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.3
Background MicroRNAs (miRNAs) function as post-transcriptional mediators for genes involved in cancer progression, including chronic lymphocytic leukemia. MiR-582-5p has been identified as a tumor suppressor in various tumors. The antioncogenic role of miR-582-5p was then validated in this study. Objective Mononuclear cells were isolated from peripheral blood samples of patients with chronic lymphocytic leukemia and healthy donors. Expression of miR-582-3p in the mononuclear cells was examined by qRT-PCR. CCK8 assay was performed to detect cell viability, and cell cycle and apoptosis were evaluated by flow cytometry. Dual luciferase activity assay was performed to determine the targeting relationship between miR-582-3p and HNRNPA1, and western blot was performed to unravel the mechanism. Results MiR-582-5p was reduced in mononuclear cells of patients with chronic lymphocytic leukemia compared to healthy donors. Forced miR-582-5p expression reduced cell viability, and promoted apoptosis of chronic lymphocytic leukemia cells. Cell cycle was arrested in G0/G1 phase via miR-582-5p mimic. MiR-582-5p bound to HNRNPA1 (heterogeneous nuclear ribonucleoprotein A1) and down-regulated its expression. Silence of HNRNPA1 decreased cell viability, promoted apoptosis, and blocked cell cycle at G0/G1 phase through up-regulation of IκBα (IkappaBalpha). Moreover, HNRNPA1 silencing attenuated the promotive effect induced by miR-582-5p inhibitor on the progression of chronic lymphocytic leukemia. Conclusion MiR-582-5p demonstrated anti-proliferative and pro-apoptotic roles in chronic lymphocytic leukemia cell growth via down-regulation of HNRNPA1 and up-regulation of IκBα, thus inactivating NF-κB. Background MicroRNAs (miRNAs) function as post-transcriptional mediators for genes involved in cancer progression, including chronic lymphocytic leukemia. MiR-582-5p has been identified as a tumor suppressor in various tumors. The antioncogenic role of miR-582-5p was then validated in this study. Objective Mononuclear cells were isolated from peripheral blood samples of patients with chronic lymphocytic leukemia and healthy donors. Expression of miR-582-3p in the mononuclear cells was examined by qRT-PCR. CCK8 assay was performed to detect cell viability, and cell cycle and apoptosis were evaluated by flow cytometry. Dual luciferase activity assay was performed to determine the targeting relationship between miR-582-3p and HNRNPA1, and western blot was performed to unravel the mechanism. Results MiR-582-5p was reduced in mononuclear cells of patients with chronic lymphocytic leukemia compared to healthy donors. Forced miR-582-5p expression reduced cell viability, and promoted apoptosis of chronic lymphocytic leukemia cells. Cell cycle was arrested in G0/G1 phase via miR-582-5p mimic. MiR-582-5p bound to HNRNPA1 (heterogeneous nuclear ribonucleoprotein A1) and down-regulated its expression. Silence of HNRNPA1 decreased cell viability, promoted apoptosis, and blocked cell cycle at G0/G1 phase through up-regulation of IκBα (IkappaBalpha). Moreover, HNRNPA1 silencing attenuated the promotive effect induced by miR-582-5p inhibitor on the progression of chronic lymphocytic leukemia. Conclusion MiR-582-5p demonstrated anti-proliferative and pro-apoptotic roles in chronic lymphocytic leukemia cell growth via down-regulation of HNRNPA1 and up-regulation of IκBα, thus inactivating NF-κB.
Jisoo Park,Eun Young Eo,Kyoung-Hee Lee,Jong Sun Park,Jae-Ho Lee,Chul-Gyu Yoo,Choon-Taek Lee,조영재 대한중환자의학회 2015 Acute and Critical Care Vol.30 No.3
Background: Arginine vasopressin (AVP) is widely used as a vasopressor agent. Some recent studies have suggested that AVP may exert an immunomodulatory effect. However, the mechanism about the anti-inflammatory effect of AVP is not well known. We investigated the effect of AVP on the ihibitor of kappa B (IκBα)/nuclear factor-kappa B (NF-κB) pathway in RAW 264.7 cells. Methods: Cultured RAW 264.7 cells were pretreated with AVP and stimulated with lipopolysaccharide (LPS). To evaluate the effect of AVP on inflammatory cytokines, the concentration of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were assessed by an enzyme-linked immunosorbent assay technique. The expression of IκBα and nuclear translocation of NF-κB p65 were measured by Western blotting, and IκB kinase (IKK) activity was analyzed by an in vitro immune complex kinase assay. To confirm the AVP effect on IκBα/NF-κB cascade and via V2 receptor, we added tolvaptan (V2 receptor antagonist) after AVP pretreatment. Results: The increase of IL-6 and TNF-α in LPS-stimulated RAW 264.7 cells was suppressed by a treatment with AVP. Pretreatment of AVP inhibited increasing of IKK activity and IκBα degradation induced by LPS in RAW 264.7 cells. Furthermore, LPS induced and NF-κB transcription was inhibited by AVP pretreatment. The observed changes in IKK activity, IκBα degradation and NF-κB transcription by AVP was abolished by tolvaptan treatment. Conclusions: Our results suggest that AVP showed anti-inflammatory effect on LPS-induced IκBα/NF-κB cascade in mouse macrophages via V2 receptors.
THE EFFECT OF AGE ON CYCLOOXYGENASE-2 GENE EXPRESSION : NF-κB ACTIVATION AND IκBα DEGRADATION
KIM, HYON-JEEN,KIM, KYU-WON,YU, BYUNG-PAL,CHUNG, HAE-YOUNG 부산대학교 유전공학연구소 2000 분자생물학 연구보 Vol.16 No.-
Increased oxidative stress resulting in the activation of NF-κB is thought to play crucial role in the expression of the cyclooxygenase-2 (COX-2), which is the is the key enzyme in proinflammatory prostanoid synthesis. In the current study, we investigated whether the aging process affects the status of the rodox-sensitive NF-κB in rat kidney, and how this age-related modulation is related to COX-2 gene expression and COX-derived reactive oxygen species (ROS). We found that the aging process strongly enhanced the activation of NF-κB and its DNA-brinding activity with an increased ROS status. Accompanied with the change in the of NF-κB and its IκBα as confirmed by the increased nuclear p65 protein. Thus, these data strongly indicated that the aging process increases NF-κB activity by downregulating IκBα. A closer examination further revealed that age-related oxidative status correlated with the increased COX-derived prostanoid biosynthetic process is mediated by the increased NF-κB-regulated COX activity. This increase in NF-κB activity was accompanied by the increased COX-2 mRNA and protein levels. Based on these data, we concluded that the age-related increase in redox-sensitive NF-κB translocation and binding activities are associated with increased ROS, and further that this transactivation was modulated by the age-related decrease of IκBα. ⓒ 2000 Elsevie Science Inc.
Characterization of anti-inflammatory effect of soybean septapeptide and its molecular mechanism
Kevin M. Lewis,Steven A. Sattler,ChulHee Kang,Hongmin Wu,Sang Geon Kim,김한복 한국미생물학회 2018 미생물학회지 Vol.54 No.3
Activation of nuclear factor kappa B (NFκB) leads to theinflammatory process. During this NFκB-dependent inflammationprocess, inducible nitric oxide synthase (iNOS) are expressedin the inflammatory cells. Our previous data indicated that aspecific septapeptide (GVAWWMY) from the soybean extractfermented by Bacillus licheniformis B1 inhibited iNOS mRNAexpression and NO production in cultured macrophage cells. Ourfurther experiments revealed that treatment of same septapeptideresulted in inhibition of LPS-induced NFκB activation byreversing degradation of IκBα, an inhibitory protein for NFκB. The molecular docking indicated that the septapeptide binds toIκB kinase β (IKKβ), and thus it can inhibit phosphorylation ofIκBα. Supporting this, the binding site for the septapeptide hasthe highest affinity (-8.7 kcal/mol) and the site was located atthe kinase domain (KD) of IKKβ, which can significantlyaffect the kinase activity of IKKβ.
Lee, Y.,Umasuthan, N.,Whang, I.,Revathy, K.S.,Lee, S.,De Zoysa, M.,Oh, C.,Kang, D.H.,Noh, J.K.,Lee, J. Academic Press 2014 FISH AND SHELLFISH IMMUNOLOGY Vol.41 No.2
IκBα is a member of IκB family, which sequesters NF-κB in an inactivate form in the cytoplasm and blocks the translocation of NF-κB to nucleus. The IκBα paralogs of rock bream (OfIκBα-A and OfIκBα-B) encoded IκBα proteins with typical features including, highly conserved IκB degradation motif, six ankyrin repeats and a PEST sequence. However, their amino acid identity and similarity were only 55.6 and 69.7%, respectively suggesting that these two genes could be the two different isoforms of IκBα. The number and size of the exons of OfIκBα-A and OfIκBα-B were conserved well with all the compared vertebrate species, although they have significantly different genomic sizes. Phylogenetic analysis revealed that OfIκBα-A and OfIκBα-B proteins cluster with IκBα family members; however, they were grouped with different subclades in IκBα family. Tissue specific expression of OfIκBα mRNA was constitutively detected in all the tested tissues, and they showed the higher transcription level in heart, liver, gill and peripheral blood cells, respectively. The injection of flagellin stimulated the mRNA expression of OfIκBα paralogs in head kidney and intestine. Moreover, the OfIκBα mRNA expression in gill and liver was significantly up-regulated by LPS, poly I:C and Edwardsiella tarda challenges. The transcription of OfIκBα was up-regulated in early-phase of injection and then rapidly restored. These results suggest that the OfIκBα paralogs might be involved in rapid immune responsive reactions in rock bream against bacterial and viral pathogens.
FK506과 cyclosporin A가 기관지상피세포, 단핵구, 림프구 및 폐포대식세포에서 Iκ Bα 분해 및 IKKα 활성에 미치는 효과
윤호일 ( Yun Ho Il ),이창훈 ( Lee Chang Hun ),이희석 ( Lee Hui Seog ),이춘택 ( Lee Chun Taeg ),김영환 ( Kim Yeong Hwan ),한성구 ( Han Seong Gu ),심영수 ( Sim Yeong Su ),유철규 ( Yu Cheol Gyu ) 대한결핵 및 호흡기학회 2003 Tuberculosis and Respiratory Diseases Vol.54 No.4
폐 상피세포에서 NF-κB/IκB 경로에 의한 염증매개 사이토카인의 발현
박계영 ( Park Gye Yeong ),이승희 ( Lee Seung Hui ),황보빈 ( Hwangbo Bin ),임재준 ( Im Jae Jun ),이춘택 ( Lee Chun Taeg ),김영환 ( Kim Yeong Hwan ),한성구 ( Han Seong Gu ),심영수 ( Sim Yeong Su ),유철규 ( Yu Cheol Gyu ) 대한결핵 및 호흡기학회 2000 Tuberculosis and Respiratory Diseases Vol.49 No.3
IκBα-SR 유전자이입이 Cisplatin, Paclitaxel에 대한 폐암세포주의 감수성에 미치는 영향
이석영 ( Lee Seog Yeong ),설자영 ( Seol Ja Yeong ),박경호 ( Park Gyeong Ho ),박근민 ( Park Geun Min ),홍용일 ( Hong Yong Il ),김철현 ( Kim Cheol Hyeon ),장승훈 ( Jang Seung Hun ),권성연 ( Kwon Seong Yeon ),유철규 ( Yu Cheol Gyu 대한결핵 및 호흡기학회 2001 Tuberculosis and Respiratory Diseases Vol.51 No.2