• 제목/요약/키워드: High Level Signal

검색결과 798건 처리시간 0.035초

Isolation and Molecular Characterization of a New CRT Binding Factor Gene from Capsella bursa-pastoris

  • Wang, Xinglong;Liu, Li;Liu, Sixiu;Sun, Xiaoqing;Deng, Zhongxiang;Pi, Yan;Sun, Xiaofen;Tang, Kexuan
    • BMB Reports
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    • 제37권5호
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    • pp.538-545
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    • 2004
  • A new CRT binding factor (CBF) gene designated Cbcbf25 was cloned from Capsella bursa-pastoris, a wild grass, by the rapid amplification of cDNA ends (RACE). The full-length cDNA of Cbcbf25 was 898 bp with a 669 bp open reading frame (ORF) encoding a putative DRE/CRT (LTRE)-binding protein of 223 amino acids. The predicted CbCBF25 protein contained a potential nuclear localization signal (NLS) in its N-terminal region followed by an AP2 DNA-binding motif and a possible acidic activation domain in the C-terminal region. Bioinformatic analysis revealed that Cbcbf25 has a high level of similarity with other CBF genes like cbf1, cbf2, and cbf3 from Arabidopsis thaliana, and Bncbf5, Bncbf7, Bncbf16, and Bncbf17 from Brassica napus. A cold acclimation assay showed that Cbcbf25 was expressed immediately after cold triggering, but this expression was transient, suggesting that it concerns cold acclimation. Our study implies that Cbcbf25 is an analogue of other CBF genes and may participate in cold-response, by for example, controlling the expression of cold-regulated genes or increasing the freezing tolerance of plants.

Sensing the Stress: the Role of the Stress-activated p38/Hog1 MAPK Signalling Pathway in Human Pathogenic Fungus Cryptococcus neoformans

  • Bahn, Yong-Sun;Heitman, Joseph
    • 한국미생물학회:학술대회논문집
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    • 한국미생물학회 2007년도 International Meeting of the Microbiological Society of Korea
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    • pp.120-122
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    • 2007
  • All living organisms use numerous signal-transduction pathways to sense and respond to their environments and thereby survive and proliferate in a range of biological niches. Molecular dissection of these signalling networks has increased our understanding of these communication processes and provides a platform for therapeutic intervention when these pathways malfunction in disease states, including infection. Owing to the expanding availability of sequenced genomes, a wealth of genetic and molecular tools and the conservation of signalling networks, members of the fungal kingdom serve as excellent model systems for more complex, multicellular organisms. Here, we employed Cryptococcus neoformans as a model system to understand how fungal-signalling circuits operate at the molecular level to sense and respond to a plethora of environmental stresses, including osmoticshock, UV, high temperature, oxidative stress and toxic drugs/metabolites. The stress-activated p38/Hog1 MAPK pathway is structurally conserved in many organisms as diverse as yeast and mammals, but its regulation is uniquely specialized in a majority of clinical Cryptococcus neoformans serotype A and D strains to control differentiation and virulence factor regulation. C. neoformans Hog1 MAPK is controlled by Pbs2 MAPK kinase (MAPKK). The Pbs2-Hog1 MAPK cascade is controlled by the fungal "two-component" system that is composed of a response regulator, Ssk1, and multiple sensor kinases, including two-component.like (Tco) 1 and Tco2. Tco1 and Tco2 play shared and distinct roles in stress responses and drug sensitivity through the Hog1 MAPK system. Furthermore, each sensor kinase mediates unique cellular functions for virulence and morphological differentiation. We also identified and characterized the Ssk2 MAPKKK upstream of the MAPKK Pbs2 and the MAPK Hog1 in C. neoformans. The SSK2 gene was identified as a potential component responsible for differential Hog1 regulation between the serotype D sibling f1 strains B3501 and B3502 through comparative analysis of their meiotic map with the meiotic segregation of Hog1-dependent sensitivity to the fungicide fludioxonil. Ssk2 is the only polymorphic component in the Hog1 MAPK module, including two coding sequence changes between the SSK2 alleles in B3501 and B3502 strains. To further support this finding, the SSK2 allele exchange completely swapped Hog1-related phenotypes between B3501 and B3502 strains. In the serotype A strain H99, disruption of the SSK2 gene dramatically enhanced capsule biosynthesis and mating efficiency, similar to pbs2 and hog1 mutations. Furthermore, ssk2, pbs2, and hog1 mutants are all hypersensitive to a variety of stresses and completely resistant to fludioxonil. Taken together, these findings indicate that Ssk2 is the critical interface protein connecting the two-component system and the Pbs2-Hog1 pathway in C. neoformans.

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Impact on Inflammation and Recovery of Skin Barrier by Nordihydroguaiaretic Acid as a Protease-Activated Receptor 2 Antagonist

  • Kim, Hyo-Young;Goo, Jung-Hyun;Joo, Yeon-Ah;Lee, Ha-Yoen;Lee, Se-Mi;Oh, Chang-Taek;Ahn, Soo-Mi;Kim, Nam-Hoon;Hwang, Jae-Sung
    • Biomolecules & Therapeutics
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    • 제20권5호
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    • pp.463-469
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    • 2012
  • Atopic dermatitis is a chronic, inflammatory disease of the skin with increased transepidermal water loss. Both an abnormal inflammatory response and a defective skin barrier are known to be involved in the pathogenesis of atopic dermatitis. Protease activated receptor 2 (PAR2) belongs to a family of G-protein coupled receptors and is activated by both trypsin and a specific agonist peptide, SLIGKV-$NH_2$. PAR2 is expressed in suprabasal layers of the epidermis and regulates inflammatory responses and barrier homeostasis. In this study, we show that nordihydroguaiaretic acid (NDGA) inhibits the PAR2-mediated signal pathway and plays a role in skin barrier recovery in atopic dermatitis. Specifically, NDGA reduces the mobilization of intracellular $Ca^{2+}$ in HaCaT keratinocytes by down-regulating inflammatory mediators, such as interleukin-8, thymus and activation-regulated chemokine and intercellular cell adhesion molecule-1 in HaCaT keratinocytes. Also, NDGA decreases the protein expression of involucrin, a differentiation maker of keratinocyte, in both HaCaT keratinocytes and normal human epidermal keratinocytes. We examined NDGA-recovered skin barrier in atopic dermatitis by using an oxazolone-induced atopic dermatitis model in hairless mice. Topical application of NDGA produced an increase in transepidermal water loss recovery and a decrease in serum IgE level, without weight loss. Accordingly, we suggest that NDGA acts as a PAR2 antagonist and may be a possible therapeutic agent for atopic dermatitis.

새로운 ABCD1 유전자의 돌연변이를 가지는 소아 대뇌형 부신백질이영양증 1례 (A Case of Childhood Cerebral Form Adrenoleukodystrophy with Novel Mutation in the ABCD1 Gene)

  • 신영림
    • 대한유전성대사질환학회지
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    • 제12권1호
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    • pp.49-53
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    • 2012
  • X 연관 부신백질이영양증(adrenoleukodystrophy, ALD)은 과산화소체베타산화과정(peroxisomal ${\beta}$-oxidation)의 장애로 매우긴사슬지방산(very long chain fatty acids, VLCFA)이 신경계의 백질과 부신피질 및 고환에 축척된다. 이 질환은 과산화소체막단백질(peroxisomal membrane protein)을 형성하는 Xq28에 위치하는 ATP-binding cassette, subfamily D, member 1 (ABCD1) 유전자 돌연변이에 의해 주로 발생한다. X 연관 ALD는 다양한 임상양상을 보이는데 전형적인 소아대뇌형 부신백질이영양증은 10세 이전의 남아에서 대뇌백질에 빠르게 진행하는 탈수초현상을 보인다. 8세 된 남자 환아로 정상발달과정을 보이던 중 초등학교 입학 후에 집중장애와 산만한 모습으로 인해 주의력결핍과다활동장애로 진단받고 치료를 받았었다. 환아는 내원 8개월 전부터 말이 어눌해 지고 걸을 때 오른 발을 끌며 자주 넘어지는 모습을 보여 내원하였고 오른쪽 상, 하지의 근력이 떨어지는 양상이 관찰되었다. 검사상 부신기능저하증 소견을 보였으며 혈청 지방산 분석검사에서는 C26:0, C42:0/C22:0, C26:0/C22:0가 증가하였다. 뇌 자기공명영상에서는 T2와 FLAIR 강조영상에서 양측의 두정후두부의 백질과 소뇌의 백질에서 대칭적으로 고신호강도를 보였다. 환아는 부신백질이영양증로 진단하였고 ABCD1 유전자 분석 검사에서 새로운 c.983delT (p.Met329CysfsX7) 돌연변이가 확인되었다. X 연관 ALD는 유전자형과 표현형에 연관성이 없으며 다양한 임상양상을 보이기 때문에 환자들마다 임상증상을 잘 관찰해야 하며 향후 유전자 기능을 좀 더 파악하고 임상증상에 영향을 주는 다른 요소에 대한 연구가 필요할 것이라 사료된다.

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식품 중 테트라싸이클린계 항생물질의 분석 (Determination of tetracycline antibiotics in food)

  • 최동미;정지윤;장문익;임무혁;박건상;홍무기
    • 분석과학
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    • 제18권3호
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    • pp.250-256
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    • 2005
  • 고속액체크로마토그라피를 이용하여 동물성 식품 중 테트라싸이클린계 항생물질의 동시분석을 시도하였다. 대상물질은 동물의 질병치료.예방, 성장촉진 및 사료효율 개선에 널리 사용되는 클로르테트라싸이클린, 독시싸이클린, 옥시테트라싸이클린 및 테트라싸이클린이었으며, 대상식품은 쇠고기, 돼지고기, 닭고기, 우유, 계란, 넙치, 우럭, 참돔, 뱀장어 및 바다가재이었다. 시료를 McIlvaine 완충액 및 20% 삼염화초산으로 추출한 후 $C_18$ 카트리지로 정제하여 고속액체크로마토그라피로 분석하였다. 이동상으로는 0.01M 수산과 아세토니트릴의 혼합용액을 85:15에서 60:40까지 기울기로 사용하였으며 UV의 검출파장은 365 nm 이었다. 평균 회수율은 71-98% 이었으며, 검출한계는 신호대 잡음비 3 이상에서 클로르테트라싸이클린은 0.022, 독시싸이클린은 0.012, 옥시테트라싸이클린은 0.012 및 테트라싸이클린은 0.009 mg/kg이었다. 대부분의 시료에서 클로르테트라싸이클린, 독시싸이클린 및 테트라싸이클린은 검출되지 않았으나, 돼지고기, 넙치 및 참돔(2시료)에서 옥시테트라싸이클린이 각각 0.04, 0.17, 0.05 및 0.08 mg/kg로 모두 잔류허용기준을 초과하지 않은 수준으로 검출되었다.

위령탕(胃苓湯) 추출물의 사람 유래 신장 메산지움 세포에서의 당뇨병성 신장 손상 개선 효과 (Wiryeongtang attenuates diabetic renal dysfunction in human renal mesangial cells)

  • 윤정주;한병혁;최은식;남궁승;정다혜;김혜윰;안유미;이윤정;강대길;이호섭
    • 대한본초학회지
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    • 제31권5호
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    • pp.71-78
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    • 2016
  • Objectives : Diabetic nephropathy is one of the most common chronic complications of diabetes and a leading cause of end-stage renal failure in the world. Mesangial cell proliferation is known as the major pathologic features such as glomerulosclerosis and renal fibrosis. Wiryeongtang (WRT) is a well-known traditional herbal formula as therapeutic agents for chronic edema and dysuresia of renal homeostasis. In the present study, we investigated whether WRT inhibits high glucose (HG)-induced renal dysfunction by TGF-β/Smads signal regulation in cultured mesangial cells.Methods : Inhibitory effect of WRT (10-50 ㎍/ml) on HG-stimulated mesangial cells proliferation and dysfunction were evaluated by [3H]-thymidine incorporation, Western blot, and RT-qPCR.Results : WRT significantly decreased HG-accelerated thymidine incorporation in human renal mesangial cell in a dose-dependent levels. WRT induced down-regulation of cyclins/CDKs and up-regulation of CDK inhibitor, p21waf1/cip1 and p27kip1 expression. In addition, HG enhanced expression of dysfunction biomarker such as collagen IV and CTGF, which was markedly attenuated by WRT. WRT decreased TGF-β1 and Smad-2/Smad-4 expression, whereas increased Smad-7 expression under HG. Furthermore, WRT inhibited HG-induced inflammatory factors level such as ICAM-1 and MCP-1 as well as NF-κB p65 nuclear translocation and intracellular ROS production.Conclusions : These results suggested that WRT may alleviate mesangial proliferation and inflammation possibly involved in renal fibrotic process, further diabetic nephropathy through disturbing TGF-β1/Smad signaling and NF-κB/ROS pathway. Thus, WRT might prove to be effective in the treatment of renal dysfunction leading to diabetic nephropathy.

PPG 2차 미분을 이용한 정상인과 당뇨병 환자의 말초혈관 탄성도 비교 (Comparison of peripheral vascular compliance between normal and diabetic groups using the second derivative of photoplethysmogram)

  • 김성우;이주형;남기창;김수찬;차은종;김덕원
    • 전자공학회논문지SC
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    • 제44권4호통권316호
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    • pp.15-20
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    • 2007
  • 현재, 우리나라 당뇨병의 유병률은 빠른 속도로 증가하고 있으며 당뇨병의 유병기간이 길수록 각종 합병증이 발생하여 더욱 심각한 증상을 나타내는데, 그 중 비만 및 고혈당, 당대사장애로 인한 당뇨병성 혈관합병증과 말초 혈관 경화증이 많이 발병하고 있는 실정이다. 따라서 본 연구에서는 광혈류량 측정법(Photoplethysmography)으로 손가락 및 발가락에서 얻어진 맥파의 2차 미분분석을 통해 연령이 비슷한 정상인 50명과 당뇨병으로 확진된 50명의 말초 혈관 탄성도를 객관적으로 비교하고자 하였다. PPG 파형의 2차 미분 분석에 사용되는 평가 인자는 a, b, c, d, e 이고, b/a는 혈관의 탄성도를 의미하며 탄성도가 떨어질수록 b/a의 절대 값은 감소하게 된다. 정상인 50명의 PPG 2차 미분 b/a값은 $-1.09{\pm}0.14$, 당뇨병 환자 50명의 PPG 2차 미분 b/a값은 $-0.81{\pm}0.09$로 정상인에 비해 당뇨병 환장의 말초혈관 탄성도가 감소하였으며, Independent t-test 검정 결과 통계적으로 유의한 차이를 보였다(p<0.05). 본 연구에서는 PPG 파형의 2차 미분 분석을 통하여 정상인과 혈관합병증 발병율이 높은 당뇨병 환자의 말초혈관 탄성도를 비교하였으며, 향후 비침습적이고 간단한 방법으로 당뇨병 환자의 말초혈관 탄성도와 혈관 경화정도를 객관적으로 평가하고 진단함으로써 당뇨병 환자들의 심혈관계질환 사전예방과 치료효과 판정에 도움을 줄 것으로 기대한다.

OFDM 시스템에서 시간 및 주파수 영역 클리핑의 Total Degradation 성능평가 (Total Degradation Performance Evaluation of the Time- and Frequency-Domain Clipping in OFDM Systems)

  • 한창식;서만중;임성빈
    • 대한전자공학회논문지TC
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    • 제44권7호통권361호
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    • pp.17-22
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    • 2007
  • OFDM (Orthogonal Frequency Division Multiplexing)시스템은 다수 반송파 전송의 특수한 형태로 볼 수 있으며 하나의 데이터열이 보다 낮은 데이터 전송률을 갖는 부반송파를 통해 전송된다. OFDM을 사용하는 중요한 이유 중 하나는 OFDM을 사용하면 주파수 선택적 페이딩이나 협대역 간섭에 대한 강건함이 증가하기 때문이다. 하지만, 시간 영역 OFDM 신호는 독립적으로 변조된 많은 부반송파들로 구성되므로 이들이 동위상으로 더해질 때 신호의 진폭이 증가하여 PAPR (Peak-to-Average Power Ratio)이 증가된다. 본 논문에서는 수신단의 구조에 변화를 주지 않으며 또한 추가적인 정보의 전송이 필요 없이 기존 수신기를 그대로 사용할 수 있는 PAPR 감소기법의 성능을 평가하였다. 이 방법은 에러 벡터 크기 (Error Vector Magnitude; EVM) 내에서 시간 영역과 주파수 영역 신호에 대하여 클리핑을 사용한 것으로 기존의 최적화 방법과 비교하여 계산량의 복잡도가 낮다. 이 기법을 비선형 증폭기를 사용하는 OFDM 시스템에서 평가하였다. 모의실험 결과, 시간 및 주파수 영역 클리핑 기반의 PAPR 감소기법은 TD (Total Degradation)관점에서 전력효율이 향상되며 증폭기의 비선형 왜곡의 영향을 줄이는 효과가 있음을 확인할 수 있었다.

MMIC 회로를 이용한 위성중계기용 30GHz대 저잡음증폭기 모듈 개발 (A 30 GHz Band Low Noise for Satellite Communications Payload using MMIC Circuits)

  • 염인복;김정환
    • 한국전자파학회논문지
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    • 제11권5호
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    • pp.796-805
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    • 2000
  • 30dB의 선형이득과 2.6dB의 잡음지수 성능을 갖는 위성통신중계기용 30GHz대 저잡음증폭기 모듈이 MMIC와 박막 MIC기술로 개발되었다. 두 종의 MMIC 회로가 저잡음증폭기 모듈에 사용되었는데, 하나는 초저잡음용 MMIC 회로이고, 다른 하나는 광대역 고이득용 MMIC 회로이다. MMIC 회로 제작에 사용된 증폭소자는 0.15$mu extrm{m}$게이트 길이를 갖는 pHEMT이다. 두 개의 MMIC 회로를 상호 연결하고 저잡음증폭기 모듈을 완성하기 위하여 박막기술을 이용하여 마이크로스트립 선로를 구현하였으며, 안정된 DC 전원 공급을 위하여 후막기술을 이용한 바이어스 회로를 개발하였다. 저잡음증폭기 모듈의 입력측은 위성중계기의 안테나로부터의 신호를 받아들이기 위하여 도파관 형태로 설계되었으며, 출력측은 주파수변환부와의 접속을 위하여 K-컨넥터로 구현되었다. 모든 제작 공정에는 실제 위성용 부품 제작 기술이 도입되었으며, 위성중계기에 탑재되는 부품에 요구되는 온도시험 및 진동시험을 실시하였다. 제작된 저잡음증폭기 모듈은 동작목표 대역인 30~31GHz에서 30dB 이상의 이득, $\pm$0.3dB의 이득평탄도, 그리고 2.6dB이하의 우수한 잡음지수를 가진 것으로 측정되었다.

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Effects of Insulin and IGFs on Phosphate Uptake in Primary Cultured Rabbit Renal Proximal Tubule Cells

  • Han, Ho-Jae;Park, Kwon-Moo
    • The Korean Journal of Physiology
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    • 제30권1호
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    • pp.63-76
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    • 1996
  • The aim of present study was to characterize phosphate uptake and to investigate the mechanism for the insulin and insulin-like growth factor(IGF) stimulation of phosphate uptake in primary cultured rabbit renal proximal tubule cells. Results were as follows : 1. The primary cultured proximal tubule cells had accumulated $6.68{\pm}0.70$ nmole phosphate/mg protein in the presence of 140 mM NaCl and $2.07{\pm}0.17$ nmole phosphate/mg protein in the presence of 140 mM KCl during a 60 minute uptake period. Raising the concentration of extracellular phosphate to 100 mM$(48.33{\pm}1.76\;pmole/mg\;protein/min)$ induced decrease in phosphate uptake compared with that in control cells maintained in 1 mM phosphate$(190.66{\pm}13.01\;pmole/mg\;protein/min)$. Optimal phosphate uptake was observed at pH 6.5 in the presence of 140 mM NaCl. Phosphate uptake at pH 7.2 and pH 7.9 decreased to $83.06{\pm}5.75%\;and\;74.61{\pm}3.29%$ of that of pH 6.5, respectively. 2. Phosphate uptake was inhibited by iodoacetic acid(IAA) or valinomycin treatment $(62.41{\pm}4.40%\;and\;12.80{\pm}1.64%\;of\;that\;of\;control,\;respectively)$. When IAA and valinomycin were added together, phosphate uptake was inhibited to $8.04{\pm}0.61%$ of that of control. Phosphate uptake by the primary proximal tubule cells was significantly reduced by ouabain treatment$(80.27{\pm}6.96%\;of\;that\;of\;control)$. Inhibition of protein and/or RNA synthesis by either cycloheximide or actinomycin D markedly attenuated phosphate uptake. 3. Extracellular CAMP and phorbol 12-myristate 13 acetate(PMA) decreased phosphate uptake in a dose-dependent manner in all experimental conditions. Treatment of cells with pertussis toxin or cholera toxin inhibited phosphate uptake. cAMP concentration between $10^{-6}\;M\;and\;10^{-4}\;M$ significantly inhibited phosphate uptake. Phosphate uptake was blocked to about 25% of that of control at 100 ng/ml PMA. 3-Isobutyl-1-methyl-xanthine(IBMX) inhibited phosphate uptake. However, in the presence of IBMX, the inhibitory effect of exogenous cAMP was not significantly potentiated. Forskolin decreased phosphate transport. Acetylsalicylic acid did not inhibit phosphate uptake. The 1,2-dioctanoyl-sn-glycorol(DAG) and 1-oleoyl-2-acetyl-sn- glycerol(OAG) showed a inhibitory effect. However, staurosporine had no effect on phosphate uptake. When PMA and staurosporine were treated together, inhibition of phosphate uptake was not observed. In conclusion, phosphate uptake is stimulated by high sodium and low phosphate and pH 6.5 in the culture medium. Membrane potential and intracellular energy levels are also an important factor fer phosphate transport. Insulin and IGF-I stimulate phosphate uptake through a mechanisms that involve do novo protein and/or RNA synthesis and decrease of intracellular cAMP level. Also protein kinase C(PKC) is may play a regulatory role in transducing the insulin and IGF-I signal for phosphate transport in primary cultured proximal tubule cells.

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