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41.

cAMP/PKA Agonist Restores the Fasting-Induced Down-Regulation of nNOS Expression in the Paraventricular Nucleus

SangBaeYoo, SeoulLee, JooYoungLee, Bom-TaeckKim, Jong-HoLee, JeongWonJahng 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2012, Vol.16 No.5 7 333-337 (5 pages)

SangBaeYoo, SeoulLee, JooYoungLee, Bom-TaeckKim, Jong-HoLee, JeongWonJahng 저
...
- 1,500원
Gene expression of neuronal nitric oxide synthase (nNOS) changes in the hypothalamic paraventricular nucleus (PVN) depending on feeding conditions, which is decreased during food deprivation and restored by refeeding, and phosphorylated cAMP response element binding protein (pCREB) was suggested to play a role in its regulation. This study was conducted to examine if the fasting-induced down-regulation of the PVN-nNOS expression is restored by activation of cAMP-dependent protein kinase A...
42.

Ser1778 of 53BP1 Plays a Role in DNA Double-strand Break Repairs

Jung-HeeLee, Hyang-MinCheong, Mi-YoungKang, Sang-YoungKim, YoonsungKang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.5 2 343-348 (6 pages)

Jung-HeeLee, Hyang-MinCheong, Mi-YoungKang, Sang-YoungKim, YoonsungKang 저
...
- 3,000원
53BP1 is an important genome stability regulator, which protects cells against double-strand breaks. Following DNA damage, 53BP1 is rapidly recruited to sites of DNA breakage, along with other DNA damage response proteins, including Ճ-H2AX, MDC1, and BRCA1. The recruitment of 53BP1 requires a tandem Tudor fold which associates with methylated histones H3 and H4. It has already been determined that the majority of DNA damage response proteins are phosphorylated by ATM and/or ATR after DNA...
43.

Expression of Endothelin-1 and Its Receptors in Cisplatin-Induced Acute Renal Failure in Mice

SeokwooLee, DowhanAhn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.4 4 149-154 (6 pages)

SeokwooLee, DowhanAhn 저
...
- 3,000원
Endothelin-1 (ET-1) is unequivocally elevated in the kidney with ischemic acute renal failure (ARF), whereas ET receptors (ETAR and ETBR) are variably expressed. Although renal functional and structural changes are similar between ischemic and nephrotoxic ARF, there are few reports on the alteration in the ET system in nephrotoxic ARF. This study was, therefore, undertaken to investigate changes in renal expression of ET-1 and its receptors in nephrotoxic ARF induced by cisplatin. Mice were...
44.

Effects of TGF-β;1 Ribbon Antisense on CCl4-induced Liver Fibrosis

Kyung-OhDoh 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.1 1 1-6 (6 pages)

Kyung-OhDoh 저
...
- 3,000원
Ribbon-type antisense oligonucleotide to TGF-Ղ1 (TGF-Ղ1 RiAS) was designed and tested to prevent or resolve the fibrotic changes induced by CCl4 injection. When Hepa1c1c7 cells were transfected with TGF-Ղ1 RiAS, the level of TGF-Ղ1 mRNA was effectively reduced. TGF-Ղ1 RiAS, mismatched RiAS, and normal saline were each injected...
45.

Gene Expression Profile in Microglia following Ischemia- Reperfusion Injury

JuHyeonOh, HyungSooHan, JaeSikPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.4 2 173-180 (8 pages)

JuHyeonOh, HyungSooHan, JaeSikPark 저
...
- 3,000원
Microglial activation is thought to play a role in the pathogenesis of many brain disorders. Therefore, understanding the response of microglia to noxious stimuli may provide insights into their role in disorders such as stroke and neurodegeneration. Many genes involved in this response have been identified individually, but not systematically. In this regards, the microarray system permitted to screen a large number of genes in biological or pathological processes. Therefore, we used microarray...
46.

Effect of Amrinone, a Selective Inhibitor of Phosphodiesterase III, on PMNs-induced

ByungKwonOh, HyoungKiKim, SooRanChoi, JinHoSong, EonSubPark, Byung 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.1 7 43-50 (8 pages)

ByungKwonOh, HyoungKiKim, SooRanChoi, JinHoSong, EonSubPark, Byung 저
...
- 3,000원
Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in a marked cardiac contractile dysfunction. Amrinone, a specific inhibitor of phosphodiesterase 3, has an antioxidant activity against PMNs. Therefore, we hypothesized that amrinone could attenuate PMNs-induced cardiac dysfunction by suppression of reactive oxygen species (ROS) produced fby PMNs. In the present study, we examined the effects of amrinone on isolated ischemic (20 min) and reperfused...
47.

Intrinsic Gating in Inward Rectifier Potassium Channels (Kir2.1) with Low Polyamine Affinity Generated by Site Directed Mutagenesis

ISo, , IAshmole, HSoh, CSPark, PJSpencer, MLeyl, PRStanfield, 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 12 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.3 3 131-142 (12 pages)

ISo, , IAshmole, HSoh, CSPark, PJSpencer, MLeyl, PRStanfield, 저
...
- 4,100원
We have studied mutant forms of Kir2.1 in which an aspartate residue (D172), important for gating by intracellular polyamines, is replaced by one of three basic residues (Arg, Lys or His). Such channels are highly selective for K+, but show inward rectification that is a shallow function of voltage compared with that found in wild type. This inward rectification occurs with a reduced affinity for spermine and persists in the absence of polyamines. Though the unitary current-voltage relation...
48.

Involvement of NAD(P)H Oxidase in a Potential Link between Diabetes and Vascular Smooth Muscle Cell Proliferation

HyeYoungJeong, MiRanYun, ChiDaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.2 9 103-109 (7 pages)

HyeYoungJeong, MiRanYun, ChiDaeKim 저
...
- 3,000원
The cellular mechanisms that contribute to the acceleration of atherosclerosis in diabetes are poorly understood. Therefore, the potential mechanisms involved in the diabetes-dependent increase in vascular smooth muscle cell (VSMC) proliferation was investigated. Using primary culture of VSMC from streptozotocin-induced diabetic rat aorta, cell proliferation assay showed two-fold increase in cell number accompanied with enhanced superoxide generation compared to normal VSMC, 2 days after...
49.

Inhibition of NF-κB Activation Increases Oxygen-Glucose Deprivation-Induced Cerebral Endothelial Cell Death

JinuLee, ChulHoonKim, KyuDaeShim, YoungSooAhn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.2 3 65-71 (7 pages)

JinuLee, ChulHoonKim, KyuDaeShim, YoungSooAhn 저
...
- 3,000원
Increasing evidences suggest that ischemia-induced vascular damage is an integral step in the cascade of the cellular and molecular events initiated by cerebral ischemia. In the present study, employing a mouse brain endothelioma-derived cell line, bEnd.3, and oxygen-glucose deprivation (OGD) as an in vitro stroke model, the role of nuclear factor kappa B (NF-κB) activation during ischemic injury was investigated. OGD was found to activate NF-κB and to induce bEnd.3 cell death in a...
50.

Functional Abnormalities of HERG Mutations in Long QT Syndrome 2 (LQT2)

MasayasuHIRAOKA 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages

대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.5 1 367-371 (5 pages)

MasayasuHIRAOKA 저
...
- 1,500원
The chromosome 7-linked long QT syndrome (LQT2) is caused by mutations in the human ether-a- go-go-related gene (HERG) that encodes the rapidly activating delayed rectifier K+ current, IKr, in cardiac myocytes. Different types of mutations have been identified in various locations of HERG channel. One of the mechanisms for the loss of normal channel function is due to membrane trafficking of channel protein. The decreased channel function in some deletion mutants appears to be due to loss of...

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