강유전체 상유전체 적층 구조에서의 음의 유전율 현상의 물리적 원리

학위논문(박사) -- 서울대학교대학원 : 공과대학 무기재료공학과, 2021.8. 박현우.1960 년 MOSFET이 개발된 이래 이 소자의 축소화는 빠르게 진행되고 있다. 2000 년대 초부터 본격적으로 개발된 나노 스케일 MOSFET 소자의 성능은 strain engineering을 통한 mobility 향상, 고유 전율 게이트 산화물 도입을 통한 EOT 감소 등 소재의 혁신과 FDSOI (Full Depeleted Silicon on Insulator), FinFET 및 GAA (Gate All Around)와 같은 새로운 구조적 혁신으로 크게 향상되었다. 그럼에도 불구하고 최근 소자의 급격한 축소화로 MOSFET 동작의 에너지 효율 저하가 심각한 문제로 대두되고 있다. MOSFET의 에너지 효율은 공급 전압 Vdd와 Off 전류를 줄임으로써 향상될 수 있다. 이를 위해서는 궁극적으로 MOSFET 소자의 On-Off 스위칭 기울기, 즉 subthreshold slope 최대화해야한다. Subthresold slope을 증가시키는 한 가지 해결책은 게이트 산화물의 커패시턴스를 높이는 것이다. 2007 년부터 게이트 산화물로 비정질 HfO2 박막을 사용하는 high-k metal gate (HKMG) 기술이 적용되어 등가 산화물 두께 (EOT)를 0.8nm까지 감소했다. 그러나 HKMG 기술을 통한 EOT 감소는 채널 Si 층과 고유 전율 산화물 사이의 SiO2 박막의 형성으로 인해 0.5nm 이하로 달성하기 어렵다는 점에서 물질적 한계가 있다. 또한 EOT가 이상적으로 0nm에 가깝게 감소하더라도 source의 전자는 열적 요동 으로 인해 임계 값 이하 영역에서 Boltzmann 분포를 갖기 때문에 실온에서 게이트 전류를 10 배 증가시키기 위해 60mV 이상의 전압을 인가해야한다. 이는 EOT가 아무리 감소하더라도 subthreshold 기울기의 역수 값이 실온에서 60mV/dec보다 낮을 수 없음을 의미하며, 이를 Boltzmann 한계라고 부른다. 따라서 Boltzmann 한계는 MOSFET 장치의 에너지 효율을 개선하는 데 근본적인 장애물로 작용한다. 그러나 2008 년 Salahuddin과 Datta는 음의 정전 용량을 갖는 게이트 산화물을 통해 Boltzmann 한계를 극복할 수 있다고 주장했다. 게이트 산화물의 커패시턴스가 음수이면 증가된 게이트 전압이 게이트 산화물 층과 채널 층으로 나뉘어 걸리지 않고 오히려 게이트 산화물에 인가되는 전압이 감소하여 채널 전압이 더 빠르게 증가한다. 즉, 게이트 산화물의 NC에 의해 전압 증폭 효과가 유도된다. 따라서 NCFET (Negatieve Capacitance Field Effect Transistor)라고 불리는 이 소자는 기존 MOSFET 소자의 에너지 효율 문제를 극복할 수 있다. 이 아이디어를 실현하기 위해 Salahuddin 그룹은 강유전성 재료가 NC 효과를 갖는 게이트 산화물의 적절한 후보가 될 수 있다고 제안했다. 이 논문에서는 강유전체에서 NC 현상의 근본 메커니즘에 대한 이론적 연구가 수행되었다. 강유전체에 대한 NC 효과의 기존 이론은 Landau-Ginzburg-Devonshire (LGD) 모델을 기반으로 한다. 이 모델은 강유전체의 1 차원적 자유 에너지를 설명하는 현상학적 모델이다. 즉, 이 모델은 강유전체에서 단일 도메인 (SD)으로 균일한 분극이 존재한다는 가정에 근거한다. 따라서 이 1-D 모델은 실제 강유전성 박막에서 흔히 볼 수 있는 다중 도메인 (MD) 구조를 무시한다. 이 점에서 본 연구는 MD 구조의 효과를 고려한 새로운 모델을 소개하고, 이로부터 MD 구조가 강유전성 박막에 형성되는 일반적인 경우에도 강유전체 (FE) – 유전체 (DE) 이중층 구조에서 NC 효과가 나타남을 밝혔다. 2014 년에 Khan et al.은 1-D LGD 모델에서의 NC 효과에 대한 직접적인 증거로 외부 저항에 직렬로 연결된 강유전체 단일층의 충방전 중에 발생하는 과도적 전압 강하 현상을 제시했다. 그러나 고전적인 강유전성 박막의 switching 이론에 따르면, switching은 균일한 스위칭이 아닌 반대 방향 domain의 핵 생성 및 DW의 이동을 통해 발생하는 것으로 잘 알려져 있다. 이 점에서 본 연구는 고전적인 switching kinetics 이론을 적용하여 과도적 전압 강하가 NC 효과가 아니라 지연된 핵 생성에 의해 발생함을 보여주었다. 또한 이 연구에서 double pulse 측정 실험을 고안하여 이 실험 결과를 1-D LGD 모델로 설명할 수 없음을 보여주었다. 다음으로 본 연구는 MD 구조를 갖는 FE-DE 적층 구조의 NC 안정화를 위한 기본 메커니즘을 제시하였다. 이 구조에서 NC 안정화의 이전 개념은 MD 구조를 고려하지 않은 현상론적 모델 인 1-D LGD 모델을 기반으로 한다. 본 연구는 FE 층의 분극-전압 (P-V) 곡선이 MD 구조를 고려하더라도 준정적 방식으로 S 모양의 곡선으로 나타날 수 있는지를 확인했다. 먼저, 이를 위해 MD 구조에서 고전적인 switching 역학을 수치적으로 재현하기 위해 Phase field simulation을 구현했으며, 그 결과 FE-DE 적층 구조에서 준 정적 NC 현상이 나타나는 것을 발견했다. 또한, MD 구조에 나타나는 NC 효과의 근본적인 메커니즘을 밝히기 위해 Bratkovsky-Levanyuk 모델로부터 새로운 해석적 모델을 유도하였다. 마지막으로 이전의 실험 결과들을 새로 제안한 모델을 통해 분석하고 1-D LGD 모델과 맞지 않는 실험 결과들을 이 MD NC 모델로부터 재 해석하였다.Since the first MOSFET (metal-oxide-semiconductor field-effect transistor) device was developed in 1960, the scaling of MOSFET devices has been rapidly progressing. The performance of the nanoscale MOSFET device, which has been developed in earnest since the early 2000s, has been dramatically improved by the material innovations such as mobility improvement through strain engineering and reduction of EOT through the introduction of the high-k gate oxide, and the development of new structures such as fully depleted silicon on insulator (FDSOI), FinFET, and Gate All Around (GAA). Nevertheless, the decrease in the energy efficiency of MOSFET operation due to the rapid scaling of the device has recently emerged as a severe problem. The energy efficiency of MOSFET device operation can be improved by reducing the supply voltage Vdd and the magnitude of the off current. For this, ultimately, the slope of the on-off switching of the MOSFET device, the subthreshold slope, should be maximized. One solution to increase the threshold slope is to increase the capacitance of the gate oxide. Since 2007, high-k metal gate (HKMG) technology in which an amorphous HfO2 thin film is used as a gate oxide has been applied, reducing the equivalent oxide thickness (EOT) to 0.8 nm. However, there is a material limitation in that the reduction of EOT through HKMG technology is challenging to achieve below 0.5 nm due to the inherent SiO2 thin film between the channel Si layer and the high-k oxide. Furthermore, even if the EOT is ideally reduced close to 0 nm, since the electrons of the source have a Boltzmann distribution in the subthreshold region due to thermal fluctuations, more than 60 mV must be applied to increase the gate current tenfold at room temperature. This fact means that no matter how much EOT is reduced, the reciprocal value of the subthreshold slope cannot be lower than 60 mV/dec at room temperature, which is called the Boltzmann limit. Therefore, the Boltzmann limit acts as a fundamental obstacle to improving the energy efficiency of MOSFET devices. However, in 2008, Salahuddin and Datta argued that the Boltzmann limit could be overcome if the capacitance of the gate oxide is negative. If the capacitance of the gate oxide is negative, the increased amount of the gate voltage is not divided into the gate oxide layer and the channel layer, but rather the voltage applied to the gate oxide is reduced so that the channel voltage increases faster than the gate voltage. The voltage amplification is induced by the negative capacitance (NC) of the gate oxide. Therefore, a MOSFET with the gate oxide having NC, called negative capacitance field effect transistor (NCFET), will overcome the energy efficiency problem. To realize this idea, Salahuddin's group proposed that ferroelectric materials could be a proper candidate for the gate oxide with the NC effect. In this dissertation, a theoretical study was conducted on the fundamental mechanism of the NC phenomenon in ferroelectrics. The conventional theory of the NC effect on ferroelectrics is based on the Landau-Ginzburg-Devonshire (LGD) model. However, this NC model is a phenomenological model that describes the 1-dimensional (1-D) free energy of ferroelectrics. The core of the theory lies in the assumption that a homogeneous polarization exists as the single domain (SD) in the ferroelectrics. Therefore, this 1-D model neglects a multi-domain (MD) structure commonly found in actual ferroelectric thin films. In this respect, this study introduces a new model that fully considers the effect of the MD structure and reveals that even in the general case where the MD structure is formed in a ferroelectric thin film, the NC effect can be realized in the ferroelectric (FE) – dielectric (DE) bilayer structure. In 2014, Khan et al. presented the transient voltage drop phenomenon while charging a single ferroelectric layer serially connected to an external resistor as direct evidence of the intrinsic NC effect in the 1-D LGD model. However, according to the classical switching kinetics theory of ferroelectric thin film, it is well known that switching occurs through nucleation and domain wall (DW) motion of the reverse domain, not the homogeneous switching. In this respect, this work showed that the transient voltage drop is caused by the delayed nucleation of the reverse domain, not the intrinsic NC effect, by applying the classical kinetics theory. This work also presented a quantitative model for this phenomenon. Furthermore, a double pulse experiment was devised, revealing that the 1-D LGD model cannot explain the experimental results. Second, this study presented a fundamental mechanism for NC stabilization of the FE-DE stacked structure in the presence of the MD state. The previous concept of the NC stabilization in the stacked structure was based on the 1-D LGD model, which is merely a phenomenological model without considering the MD structure. This work was initially aimed to investigate whether the polarization – voltage (P-V) curve of the FE layer can exhibit an S-shaped curve in a quasi-static manner even when the MD structure is considered. For this purpose, a phase-field simulation was implemented to reproduce the classical switching kinetics in the MD structure numerically, and as a result, it was found that the quasi-static NC phenomenon appears in the FE-DE stacked structure. Furthermore, to reveal the fundamental mechanism for the NC effect occurring in the MD structure, the analytical model for the NC effect in the MD structure was derived from the Bratkovsky-Levanyuk model, a previous study on the FE-DE stacked structure with the MD structure.1. Introduction 1 1.1. Overview and issues on negative capacitance 1 1.2. Objective and chapter overview 8 1.3. References 10 2. Literature 12 2.1. Basic theory of negative capacitance 12 2.2. Depolarization in ferroelectric thin films 18 2.3. Tunnel switching behavior in FE/DE bilayer structure and frustration of negative capacitance 20 2.4. References 26 3. Voltage drop in a ferroelectric sinlge layer by retarded domain nucleation 28 3.1. Introduction 28 3.2. Experimental 31 3.3. Results and Discussions 32 3.3.1 Transient voltage drop model based on the classical switching kinetics 32 3.3.2 Comparison with the experimental results of the transient voltage drop effect 47 3.3.3 Double pulse experiment defying the L-K model 52 3.3.4 Simulated P-V loops from two models; L-K model, and retarded nucleation model 61 3.4. Conclusion 63 3.5. References 65 4. Modeling of negative capacitance in ferroelectrics with multi-domain structures 67 4.1. Introduction 67 4.2. Results and Discussions 74 4.2.1 Basic concepts of NC from the ferroelectric thin film 74 4.2.2 Charge injection and a permanent ferroelectric switching 85 4.2.3 Stabilization of NC by scaling device dimensions 87 4.2.4 MIMFM vs. MFIM (MIFIM) system 90 4.2.5 Chensky-Tarasenko Formalism of MIFIM system 94 4.2.6 Quasi-static NC from the multi-domain structure 101 4.2.7 Effect of ferroelectric thickness on the static NC 108 4.2.8 Analytic model for static NC from the multi-domain state 119 4.2.9 Capacitance matching and internal voltage boosting 155 4.2.10 Negative capacitance in a sinusoidal domain structure 158 4.3. Conclusion 170 4.4. References 172 5. Conclusion 185 Abstract (in Korean) 189박

Mortenson Center 해외 연수보고서

서울대학교 도서관 해외 연수프로그램의 일환으로 본인은 2009년 9월 14일부터 10월 29일까지 7주간 미국 일리노이 주립대학 도서관 안에 위치한 Mortenson Center에서 실시하고 있는 International Library Programs에 참가하여 연수 교육을 받았다. 1991년에 시작된 이 프로그램을 통해서 현재까지 89개국에서 700여명이 넘는 사서 또는 도서관 관련 전문직 종사자들이 교육을 받았는데, 이 프로그램은 사서 또는 도서관 관련 전문직 종사자를 대상으로 7주간이라는 장기간의 도서관 교육을 하는 전 세계에서 유일한 교육 프로그램이다. 작년까지 이 프로그램은 9월초에 시작하여 11월초에 걸쳐 8주간 이루어졌었으나 금년부터는 7주 동안 시행되었다

Transcriptional activation of NEMO and cell survival mediated by Nrf2

학위논문 (석사)-- 서울대학교 대학원 : 약학대학 약학과, 2018. 2. 김상건.Nrf2는 세포 생존의 중심적인 조절자로서, 활성 산소 제거를 통하여 세포사를 억제한다. NF-kB essential modulator (NEMO)는 NF-kB를 활성화 시킴으로써 세포 생존 단백질의 발현을 촉진한다. Nrf2와 NEMO 모두 세포 생존에 관여하지만, 두 단백질 사이의 관계에 대해서는 아직 연구된 바가 없다. 본 연구는 Nrf2의 새로운 타겟 유전자로 NEMO를 제시하였다. Nrf2가 NEMO의 전사에 대한 역할과 그 기능적 결과에 대해 조사하였다. GEO (Gene expression omnibus) 분석을 통하여 Nrf2 knockout 마우스에서 감소하는 유전자와 Keap1 knockout 마우스에서 증가하는 유전자의 교집합에서 IKBKG를 도출하였다. Nrf2를 활성화시켰을 때, TNFα가 조절되는지 보기 위하여 sulforaphane을 사용하여 Nrf2를 활성화 시킨 결과, IkBα의 분해가 촉진되는 것을 관찰하였고 이를 통해 RelA가 증가하는 것을 관찰하였다. Nrf2가 knock out된 쥐의 간에서 NEMO가 크게 감소하였다. 반대로 Nrf2를 과발현 하였을 때에는, NEMO mRNA의 발현이 증가하였고, Nrf2 siRNA를 이용하여 knock down 시켰을 때에는 다시 감소하였다. CHIP sequencing과 크로마틴 면역 침강법을 통해 Nrf2가 직접 NEMO를 전사적으로 활성화 한다는 것을 증명하였다. Nrf2에 의한 NEMO mRNA의 증가가 단백질 수준에서도 일어나는 것을 보였다. 세포 죽음을 수반하는 다양한 질환 모델에서 IKBKG의 발현을 관찰하였다. 아세타미노펜 독성으로 내원한 환자들의 마이크로어레이에서는 NEMO와 Nrf2가 감소되어 있는 현상을 관찰하였고, 독성 용량의 아세타미노펜을 투여한 쥐에서도 NEMO와 Nrf2가 낮은 발현을 보였다. 반대로, 알코올성 간염 환자의 간에서는 NEMO가 적응적으로 증가하였다. 세포 죽음 시에 염증이 필수적으로 수반되기 때문에, Nrf2를 통한 NEMO의 활성화가 마크로파지의 분화에 영향을 주는 지 탐구하였으나, M1, M2 마크로파지로의 분화에 영향을 주지 않았다. 본 연구에서는, Nrf2가 전사적으로 NEMO 유전자의 발현을 촉진한다는 것을 새롭게 규명하였다.I. 서론 1 II. 실험재료 및 방법 3 1. 시약 및 항체 3 2. 세포배양 3 3. 실험동물 3 4. 세포 분획의 분리 4 5. 면역 화학적 분석 (Immunoblotting) 3 6. 실시간 역전사 중합 효소 연쇄 반응법 (Real-Time RT-PCR) 5 7. 형질도입 (Transfection) 5 8. siRNA 트랜스펙션 (Transfection) 6 9. 크로마틴 면역침강법 (Chromatin Immunoprecipitation, ChIP) 6 10. 생물정보학적 분석 7 11. 통계처리 7 III. 실험 결과 8 VI. 결론 및 고찰 21 V. 참고 문헌 25 ABSTRACT 29Maste

Transepithelial Bicarbonate Secretion: Lessons from the Pancreas.

Many cystic fibrosis transmembrane conductance regulator (CFTR)-expressing epithelia secrete bicarbonate (HCO(3)(-))-containing fluids. Recent evidence suggests that defects in epithelial bicarbonate secretion are directly involved in the pathogenesis of cystic fibrosis, in particular by building up hyperviscous mucus in the ductal structures of the lung and pancreas. Pancreatic juice is one of the representative fluids that contain a very high concentration of bicarbonate among bodily fluids that are secreted from CFTR-expressing epithelia. We introduce up-to-date knowledge on the basic principles of transepithelial bicarbonate transport by showing the mechanisms involved in pancreatic bicarbonate secretion. The model of pancreatic bicarbonate secretion described herein may also apply to other exocrine epithelia. As a central regulator of bicarbonate transport at the apical membrane, CFTR plays an essential role in both direct and indirect bicarbonate secretion. The major role of CFTR in bicarbonate secretion would be variable depending on the tissue and cell type. For example, in epithelial cells that produce a low concentration of bicarbonate-containing fluid (up to 80 mm), either CFTR-dependent Cl(-)/HCO(3)(-) exchange or CFTR anion channel with low bicarbonate permeability would be sufficient to generate such fluid. However, in cells that secrete high-bicarbonate-containing fluids, a highly selective CFTR bicarbonate channel activity is required. Therefore, understanding the molecular mechanism of transepithelial bicarbonate transport and the role of CFTR in each specific epithelium will provide therapeutic strategies to recover from epithelial defects induced by hyposecretion of bicarbonate in cystic fibrosis.ope

Molecular mechanism of pancreatic and salivary gland fluid and HCO3 secretion

Fluid and HCO(3)(-) secretion is a vital function of all epithelia and is required for the survival of the tissue. Aberrant fluid and HCO(3)(-) secretion is associated with many epithelial diseases, such as cystic fibrosis, pancreatitis, Sjögren's syndrome, and other epithelial inflammatory and autoimmune diseases. Significant progress has been made over the last 20 years in our understanding of epithelial fluid and HCO(3)(-) secretion, in particular by secretory glands. Fluid and HCO(3)(-) secretion by secretory glands is a two-step process. Acinar cells secrete isotonic fluid in which the major salt is NaCl. Subsequently, the duct modifies the volume and electrolyte composition of the fluid to absorb the Cl(-) and secrete HCO(3)(-). The relative volume secreted by acinar and duct cells and modification of electrolyte composition of the secreted fluids varies among secretory glands to meet their physiological functions. In the pancreas, acinar cells secrete a small amount of NaCl-rich fluid, while the duct absorbs the Cl(-) and secretes HCO(3)(-) and the bulk of the fluid in the pancreatic juice. Fluid secretion appears to be driven by active HCO(3)(-) secretion. In the salivary glands, acinar cells secrete the bulk of the fluid in the saliva that is driven by active Cl(-) secretion and contains high concentrations of Na(+) and Cl(-). The salivary glands duct absorbs both the Na(+) and Cl(-) and secretes K(+) and HCO(3)(-). In this review, we focus on the molecular mechanism of fluid and HCO(3)(-) secretion by the pancreas and salivary glands, to highlight the similarities of the fundamental mechanisms of acinar and duct cell functions, and to point out the differences to meet gland-specific secretions.ope

Mechanisms of CFTR Functional Variants That Impair Regulated Bicarbonate Permeation and Increase Risk for Pancreatitis but Not for Cystic Fibrosis.

CFTR is a dynamically regulated anion channel. Intracellular WNK1-SPAK activation causes CFTR to change permeability and conductance characteristics from a chloride-preferring to bicarbonate-preferring channel through unknown mechanisms. Two severe CFTR mutations (CFTRsev) cause complete loss of CFTR function and result in cystic fibrosis (CF), a severe genetic disorder affecting sweat glands, nasal sinuses, lungs, pancreas, liver, intestines, and male reproductive system. We hypothesize that those CFTR mutations that disrupt the WNK1-SPAK activation mechanisms cause a selective, bicarbonate defect in channel function (CFTRBD) affecting organs that utilize CFTR for bicarbonate secretion (e.g. the pancreas, nasal sinus, vas deferens) but do not cause typical CF. To understand the structural and functional requirements of the CFTR bicarbonate-preferring channel, we (a) screened 984 well-phenotyped pancreatitis cases for candidate CFTRBD mutations from among 81 previously described CFTR variants; (b) conducted electrophysiology studies on clones of variants found in pancreatitis but not CF; (c) computationally constructed a new, complete structural model of CFTR for molecular dynamics simulation of wild-type and mutant variants; and (d) tested the newly defined CFTRBD variants for disease in non-pancreas organs utilizing CFTR for bicarbonate secretion. Nine variants (CFTR R74Q, R75Q, R117H, R170H, L967S, L997F, D1152H, S1235R, and D1270N) not associated with typical CF were associated with pancreatitis (OR 1.5, p = 0.002). Clones expressed in HEK 293T cells had normal chloride but not bicarbonate permeability and conductance with WNK1-SPAK activation. Molecular dynamics simulations suggest physical restriction of the CFTR channel and altered dynamic channel regulation. Comparing pancreatitis patients and controls, CFTRBD increased risk for rhinosinusitis (OR 2.3, p<0.005) and male infertility (OR 395, p<<0.0001). WNK1-SPAK pathway-activated increases in CFTR bicarbonate permeability are altered by CFTRBD variants through multiple mechanisms. CFTRBD variants are associated with clinically significant disorders of the pancreas, sinuses, and male reproductive system.ope

Reprogramming anchorage dependency by adherent-to-suspension transition promotes metastatic dissemination

Background: Although metastasis is the foremost cause of cancer-related death, a specialized mechanism that reprograms anchorage dependency of solid tumor cells into circulating tumor cells (CTCs) during metastatic dissemination remains a critical area of challenge. Methods: We analyzed blood cell-specific transcripts and selected key Adherent-to-Suspension Transition (AST) factors that are competent to reprogram anchorage dependency of adherent cells into suspension cells in an inducible and reversible manner. The mechanisms of AST were evaluated by a series of in vitro and in vivo assays. Paired samples of primary tumors, CTCs, and metastatic tumors were collected from breast cancer and melanoma mouse xenograft models and patients with de novo metastasis. Analyses of single-cell RNA sequencing (scRNA-seq) and tissue staining were performed to validate the role of AST factors in CTCs. Loss-of-function experiments were performed by shRNA knockdown, gene editing, and pharmacological inhibition to block metastasis and prolong survival. Results: We discovered a biological phenomenon referred to as AST that reprograms adherent cells into suspension cells via defined hematopoietic transcriptional regulators, which are hijacked by solid tumor cells to disseminate into CTCs. Induction of AST in adherent cells 1) suppress global integrin/ECM gene expression via Hippo-YAP/TEAD inhibition to evoke spontaneous cell-matrix dissociation and 2) upregulate globin genes that prevent oxidative stress to acquire anoikis resistance, in the absence of lineage differentiation. During dissemination, we uncover the critical roles of AST factors in CTCs derived from patients with de novo metastasis and mouse models. Pharmacological blockade of AST factors via thalidomide derivatives in breast cancer and melanoma cells abrogated CTC formation and suppressed lung metastases without affecting the primary tumor growth. Conclusion: We demonstrate that suspension cells can directly arise from adherent cells by the addition of defined hematopoietic factors that confer metastatic traits. Furthermore, our findings expand the prevailing cancer treatment paradigm toward direct intervention within the metastatic spread of cancer. © 2023. The Author(s).ope

PDZ-based adaptor proteins in epithelial anion transport and VIP receptor regulation

Polarized protein deposition at the apical and basolateral membranes of epithelial cells is critical for the asymmetrical transport of ions and fluids across the epithelia. PDZ-based modular adaptor proteins are expressed in the junctional areas in epithelial cells and are generally part of a molecular scaffold that determines the localization and activity of ion channels, receptors, and other signaling molecules to their correct spatial arrangement for proper response to diverse stimuli. Hence, understanding the regulatory mechanisms of channels and receptors via PDZ-based adaptors will provide valuable insights into the physiology of epithelial cells as well as pathophysiology of many human diseases including cystic fibrosis.ope

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