|
1
|
Marban E: Cardiac channelopathies. Nature.
415:213–218. 2002. View
Article : Google Scholar : PubMed/NCBI
|
|
2
|
Platt D and Griggs R: Skeletal muscle
channelopathies: new insights into the periodic paralyses and
nondystrophic myotonias. Curr Opin Neurol. 22:524–531. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
3
|
Catterall WA, Dib-Hajj S, Meisler MH and
Pietrobon D: Inherited neuronal ion channelopathies: new windows on
complex neurological diseases. J Neurosci. 28:11768–11777. 2008.
View Article : Google Scholar : PubMed/NCBI
|
|
4
|
Planells-Cases R and Jentsch TJ: Chloride
channelopathies. Biochim Biophys Acta. 1792:173–189. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
5
|
Rolim AL, Lindsey SC, Kunii IS, et al: Ion
channelopathies in endocrinology: recent genetic findings and
pathophysiological insights. Arq Bras Endocrinol Metabol.
54:673–681. 2010. View Article : Google Scholar
|
|
6
|
Lehen’kyi V, Shapovalov G, Skryma R and
Prevarskaya N: Ion channels and transporters in cancer. 5 Ion
channels in control of cancer and cell apoptosis. Am J Physiol Cell
Physiol. 301:C1281–C1289. 2011. View Article : Google Scholar
|
|
7
|
Kunzelmann K: Ion channels and cancer. J
Membr Biol. 205:159–173. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Hoffmann EK and Lambert IH: Ion channels
and transporters in the development of drug resistance in cancer
cells. Philos Trans R Soc Lond B Biol Sci. 369:201301092014.
View Article : Google Scholar : PubMed/NCBI
|
|
9
|
Lang F and Stournaras C: Ion channels in
cancer: future perspectives and clinical potential. Philos Trans R
Soc Lond B Biol Sci. 369:201301082014. View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Li M and Xiong ZG: Ion channels as targets
for cancer therapy. Int J Physiol Pathophysiol Pharmacol.
3:156–166. 2011.PubMed/NCBI
|
|
11
|
Arcangeli A, Crociani O, Lastraioli E,
Masi A, Pillozzi S and Becchetti A: Targeting ion channels in
cancer: a novel frontier in antineoplastic therapy. Curr Med Chem.
16:66–93. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
12
|
Conti M: Targeting ion channels for new
strategies in cancer diagnosis and therapy. Curr Clin Pharmacol.
2:135–144. 2007. View Article : Google Scholar
|
|
13
|
Bortner CD and Cidlowski JA: Ion channels
and apoptosis in cancer. Philos Trans R Soc Lond B Biol Sci.
369:201301042014. View Article : Google Scholar : PubMed/NCBI
|
|
14
|
Becchetti A, Munaron L and Arcangeli A:
The role of ion channels and transporters in cell proliferation and
cancer. Front Physiol. 4:3122013. View Article : Google Scholar : PubMed/NCBI
|
|
15
|
Prevarskaya N, Skryma R, Bidaux G,
Flourakis M and Shuba Y: Ion channels in death and differentiation
of prostate cancer cells. Cell Death Differ. 14:1295–1304. 2007.
View Article : Google Scholar : PubMed/NCBI
|
|
16
|
Lang F, Foller M, Lang KS, et al: Ion
channels in cell proliferation and apoptotic cell death. J Membr
Biol. 205:147–157. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Lang F, Foller M, Lang K, et al: Cell
volume regulatory ion channels in cell proliferation and cell
death. Methods Enzymol. 428:209–225. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
18
|
Urrego D, Tomczak AP, Zahed F, Stuhmer W
and Pardo LA: Potassium channels in cell cycle and cell
proliferation. Philos Trans R Soc Lond B Biol Sci.
369:201300942014. View Article : Google Scholar : PubMed/NCBI
|
|
19
|
Blackiston DJ, McLaughlin KA and Levin M:
Bioelectric controls of cell proliferation: ion channels, membrane
voltage and the cell cycle. Cell Cycle. 8:3527–3536. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
20
|
Abdul M and Hoosein N: Expression and
activity of potassium ion channels in human prostate cancer. Cancer
Lett. 186:99–105. 2002. View Article : Google Scholar : PubMed/NCBI
|
|
21
|
Nilius B, Eggermont J, Voets T and
Droogmans G: Volume-activated Cl− channels. Gen
Pharmacol. 27:1131–1140. 1996. View Article : Google Scholar : PubMed/NCBI
|
|
22
|
Shen MR, Yang TP and Tang MJ: A novel
function of BCL-2 overexpression in regulatory volume decrease.
Enhancing swelling-activated Ca(2+) entry and Cl(−) channel
activity. J Biol Chem. 277:15592–15599. 2002. View Article : Google Scholar : PubMed/NCBI
|
|
23
|
Duan DD: The CLC-3 chloride channels in
cardiovascular disease. Acta Pharmacol Sin. 32:675–684. 2011.
View Article : Google Scholar : PubMed/NCBI
|
|
24
|
Mao J, Chen L, Xu B, et al: Suppression of
CLC-3 channel expression reduces migration of nasopharyngeal
carcinoma cells. Biochem Pharmacol. 75:1706–1716. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
25
|
Lemonnier L, Shuba Y, Crepin A, et al:
Bcl-2-dependent modulation of swelling-activated Cl−
current and CLC-3 expression in human prostate cancer epithelial
cells. Cancer Res. 64:4841–4848. 2004. View Article : Google Scholar : PubMed/NCBI
|
|
26
|
Habela CW, Olsen ML and Sontheimer H: CLC3
is a critical regulator of the cell cycle in normal and malignant
glial cells. J Neurosci. 28:9205–9217. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
27
|
Wang GX, Hatton WJ, Wang GL, et al:
Functional effects of novel anti-CLC-3 antibodies on native
volume-sensitive osmolyte and anion channels in cardiac and smooth
muscle cells. Am J Physiol Heart Circ Physiol. 285:H1453–H1463.
2003.PubMed/NCBI
|
|
28
|
Do CW, Lu W, Mitchell CH and Civan MM:
Inhibition of swelling-activated Cl− currents by
functional anti-CLC-3 antibody in native bovine non-pigmented
ciliary epithelial cells. Invest Ophthalmol Vis Sci. 46:948–955.
2005. View Article : Google Scholar : PubMed/NCBI
|
|
29
|
Zhou JG, Ren JL, Qiu QY, He H and Guan YY:
Regulation of intracellular CI− concentration through
volume-regulated CLC-3 chloride channels in A10 vascular smooth
muscle cells. J Biol Chem. 280:7301–7308. 2005. View Article : Google Scholar
|
|
30
|
Duran C, Thompson CH, Xiao Q and Hartzell
HC: Chloride channels: often enigmatic, rarely predictable. Annu
Rev Physiol. 72:95–121. 2010. View Article : Google Scholar :
|
|
31
|
Guzman RE, Grieschat M, Fahlke C and
Alekov AK: CLC-3 is an intracellular chloride/proton exchanger with
large voltage-dependent nonlinear capacitance. ACS Chem Neurosci.
4:994–1003. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
32
|
Scheel O, Zdebik AA, Lourdel S and Jentsch
TJ: Voltage-dependent electrogenic chloride/proton exchange by
endosomal CLC proteins. Nature. 436:424–427. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
33
|
Picollo A and Pusch M: Chloride/proton
antiporter activity of mammalian CLC proteins CLC-4 and CLC-5.
Nature. 436:420–423. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
34
|
Hara-Chikuma M, Yang B, Sonawane ND,
Sasaki S, Uchida S and Verkman AS: CLC-3 chloride channels
facilitate endosomal acidification and chloride accumulation. J
Biol Chem. 280:1241–1247. 2005. View Article : Google Scholar
|
|
35
|
Rajagopal A and Simon SM: Subcellular
localization and activity of multidrug resistance proteins. Mol
Biol Cell. 14:3389–3399. 2003. View Article : Google Scholar : PubMed/NCBI
|
|
36
|
Weylandt KH, Nebrig M, Jansen-Rosseck N,
et al: CLC-3 expression enhances etoposide resistance by increasing
acidification of the late endocytic compartment. Mol Cancer Ther.
6:979–986. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
37
|
Su J, Xu Y, Zhou L, et al: Suppression of
chloride channel 3 expression facilitates sensitivity of human
glioma U251 cells to cisplatin through concomitant inhibition of
Akt and autophagy. Anat Rec (Hoboken). 296:595–603. 2013.
View Article : Google Scholar
|
|
38
|
Xu Y, Zheng H, Kang JS, et al:
5-Nitro-2-(3-phenylpropylamino) benzoic acid induced drug
resistance to cisplatin in human erythroleukemia cell lines. Anat
Rec (Hoboken). 294:945–952. 2011. View Article : Google Scholar
|
|
39
|
Xu B, Mao J, Wang L, et al: CLC-3 chloride
channels are essential for cell proliferation and cell cycle
progression in nasopharyngeal carcinoma cells. Acta Biochim Biophys
Sin (Shanghai). 42:370–380. 2010. View Article : Google Scholar
|
|
40
|
Zhang H, Zhu L, Zuo W, et al: The CLC-3
chloride channel protein is a downstream target of cyclin D1 in
nasopharyngeal carcinoma cells. Int J Biochem Cell Biol.
45:672–683. 2013. View Article : Google Scholar
|
|
41
|
Sontheimer H: An unexpected role for ion
channels in brain tumor metastasis. Exp Biol Med (Maywood).
233:779–791. 2008. View Article : Google Scholar
|
|
42
|
Wang L, Ma W, Zhu L, et al: CLC-3 is a
candidate of the channel proteins mediating acid-activated chloride
currents in nasopharyngeal carcinoma cells. Am J Physiol Cell
Physiol. 303:C14–C23. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
43
|
Li M, Wu DB and Wang J: Effects of
volume-activated chloride channels on the invasion and migration of
human endometrial cancer cells. Eur J Gynaecol Oncol. 34:60–64.
2013.PubMed/NCBI
|
|
44
|
Wen PY and Kesari S: Malignant gliomas in
adults. N Engl J Med. 359:492–507. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
45
|
Lui VC, Lung SS, Pu JK, Hung KN and Leung
GK: Invasion of human glioma cells is regulated by multiple
chloride channels including CLC-3. Anticancer Res. 30:4515–4524.
2010.PubMed/NCBI
|
|
46
|
Olsen ML, Schade S, Lyons SA, Amaral MD
and Sontheimer H: Expression of voltage-gated chloride channels in
human glioma cells. J Neurosci. 23:5572–5582. 2003.PubMed/NCBI
|
|
47
|
Jantaratnotai N and McLarnon JG: Calcium
dependence of purinergic subtype P2Y1 receptor
modulation of C6 glioma cell migration. Neurosci Lett. 497:80–84.
2011. View Article : Google Scholar : PubMed/NCBI
|
|
48
|
Montana V and Sontheimer H: Bradykinin
promotes the chemotactic invasion of primary brain tumors. J
Neurosci. 31:4858–4867. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
49
|
Cuddapah VA and Sontheimer H: Molecular
interaction and functional regulation of CLC-3 by
Ca2+/calmodulin-dependent protein kinase II (CaMKII) in
human malignant glioma. J Biol Chem. 285:11188–11196. 2010.
View Article : Google Scholar : PubMed/NCBI
|
|
50
|
Huang P, Liu J, Di A, et al: Regulation of
human CLC-3 channels by multifunctional
Ca2+/calmodulin-dependent protein kinase. J Biol Chem.
276:20093–20100. 2001. View Article : Google Scholar : PubMed/NCBI
|
|
51
|
Cuddapah VA, Turner KL, Seifert S and
Sontheimer H: Bradykinin-induced chemotaxis of human gliomas
requires the activation of KCa3.1 and CLC-3. J Neurosci.
33:1427–1440. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
52
|
Habela CW and Sontheimer H: Cytoplasmic
volume condensation is an integral part of mitosis. Cell Cycle.
6:1613–1620. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
53
|
Cuddapah VA, Habela CW, Watkins S, Moore
LS, Barclay TT and Sontheimer H: Kinase activation of CLC-3
accelerates cytoplasmic condensation during mitotic cell rounding.
Am J Physiol Cell Physiol. 302:C527–C538. 2012. View Article : Google Scholar :
|
|
54
|
Wang LW, Chen LX and Jacob T: CLC-3
expression in the cell cycle of nasopharyngeal carcinoma cells.
Sheng Li Xue Bao. 56:230–236. 2004.PubMed/NCBI
|
|
55
|
Ye D, Zhang HF, Zhu LY, Wang LW and Chen
LX: CLC-3 siRNA inhibits regulatory volume decrease in
nasopharyngeal carcinoma cells. Nan Fang Yi Ke Da Xue Xue Bao.
31:216–220. 2011.(In Chinese). PubMed/NCBI
|
|
56
|
Yang L, Ye D, Ye W, et al: CLC-3 Is A main
component of background chloride channels activated under isotonic
conditions by autocrine ATP in nasopharyngeal varcinoma cells. J
Cell Physiol. 226:2516–2526. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
57
|
Zhu L, Yang H, Zuo W, et al: Differential
expression and roles of volume-activated chloride channels in
control of growth of normal and cancerous nasopharyngeal epithelial
cells. Biochem Pharmacol. 83:324–334. 2012. View Article : Google Scholar
|
|
58
|
Raghunand N, Martinez-Zaguilan R, Wright
SH and Gillies RJ: pH and drug resistance. II Turnover of acidic
vesicles and resistance to weakly basic chemotherapeutic drugs.
Biochem Pharmacol. 57:1047–1058. 1999. View Article : Google Scholar
|
|
59
|
Hoffmann EK, Lambert IH and Pedersen SF:
Physiology of cell volume regulation in vertebrates. Physiol Rev.
89:193–277. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
60
|
Lang F: Mechanisms and significance of
cell volume regulation. J Am Coll Nutr. 26:S613–S623. 2007.
View Article : Google Scholar
|
|
61
|
Sardini A, Amey JS, Weylandt KH, Nobles M,
Valverdez MA and Higgins CF: Cell volume regulation and
swelling-activated chloride channels. Biochim Biophys Acta.
1618:153–162. 2003. View Article : Google Scholar
|
|
62
|
Wondergem R, Gong W, Monen SH, et al:
Blocking swelling-activated chloride current inhibits mouse liver
cell proliferation. J Physiol. 532:661–672. 2001. View Article : Google Scholar : PubMed/NCBI
|
|
63
|
Nilius B, Prenen J, Kamouchi M, Viana F,
Voets T and Droogmans G: Inhibition by mibefradil, a novel calcium
channel antagonist, of Ca(2+)- and volume-activated Cl−
channels in macrovascular endothelial cells. Br J Pharmacol.
121:547–555. 1997. View Article : Google Scholar : PubMed/NCBI
|
|
64
|
Liang W, Huang L, Zhao D, et al:
Swelling-activated Cl− currents and intracellular CLC-3
are involved in proliferation of human pulmonary artery smooth
muscle cells. J Hypertens. 32:318–330. 2014. View Article : Google Scholar
|
|
65
|
Shen MR, Droogmans G, Eggermont J, Voets
T, Ellory JC and Nilius B: Differential expression of
volume-regulated anion channels during cell cycle progression of
human cervical cancer cells. J Physiol. 529:385–394. 2000.
View Article : Google Scholar : PubMed/NCBI
|
|
66
|
Duan D, Winter C, Cowley S, Hume JR and
Horowitz B: Molecular identification of a volume-regulated chloride
channel. Nature. 390:417–421. 1997. View
Article : Google Scholar : PubMed/NCBI
|
|
67
|
Stobrawa SM, Breiderhoff T, Takamori S,
Engel D, Schweizer M, Zdebik AA, Bösl MR, Ruether K, Jahn H,
Draguhn A, Jahn R and Jentsch TJ: Disruption of CLC-3, a chloride
channel expressed on synaptic vesicles, leads to a loss of the
hippocampus. Neuron. 29:185–196. 2001. View Article : Google Scholar : PubMed/NCBI
|
|
68
|
Yamamoto-Mizuma S, Wang GX, Liu LL, et al:
Altered properties of volume-sensitive osmolyte and anion channels
(VSOACs) and membrane protein expression in cardiac and smooth
muscle myocytes from Clcn3−/− mice. J Physiol.
557:439–456. 2004. View Article : Google Scholar : PubMed/NCBI
|
|
69
|
Xiong D, Heyman NS, Airey J, et al:
Cardiac-specific, inducible CLC-3 gene deletion eliminates native
volume-sensitive chloride channels and produces myocardial
hypertrophy in adult mice. J Mol Cell Cardiol. 48:211–219. 2010.
View Article : Google Scholar :
|
|
70
|
Wang GL, Wang XR, Lin MJ, He H, Lan XJ and
Guan YY: Deficiency in CLC-3 chloride channels prevents rat aortic
smooth muscle cell proliferation. Circ Res. 91:E28–E32. 2002.
View Article : Google Scholar : PubMed/NCBI
|
|
71
|
Tang YB, Liu YJ, Zhou JG, Wang GL, Qiu QY
and Guan YY: Silence of CLC-3 chloride channel inhibits cell
proliferation and the cell cycle via G/S phase arrest in rat
basilar arterial smooth muscle cells. Cell Prolif. 41:775–785.
2008. View Article : Google Scholar : PubMed/NCBI
|
|
72
|
Rouzaire-Dubois B, O’Regan S and Dubois
JM: Cell size-dependent and independent proliferation of rodent
neuroblastoma x glioma cells. J Cell Physiol. 203:243–250. 2005.
View Article : Google Scholar
|
|
73
|
Dubois JM and Rouzaire-Dubois B: The
influence of cell volume changes on tumour cell proliferation. Eur
Biophys J. 33:227–232. 2004. View Article : Google Scholar
|
|
74
|
Van der Wijk T, De Jonge HR and Tilly BC:
Osmotic cell swelling-induced ATP release mediates the activation
of extracellular signal-regulated protein kinase (Erk)-1/2 but not
the activation of osmo-sensitive anion channels. Biochem J.
343:579–586. 1999. View Article : Google Scholar : PubMed/NCBI
|
|
75
|
Sadoshima J, Qiu Z, Morgan JP and Izumo S:
Tyrosine kinase activation is an immediate and essential step in
hypotonic cell swelling-induced ERK activation and c-fos gene
expression in cardiac myocytes. EMBO J. 15:5535–5546.
1996.PubMed/NCBI
|
|
76
|
Modi PK, Komaravelli N, Singh N and Sharma
P: Interplay between MEK-ERK signaling, cyclin D1 and
cyclin-dependent kinase 5 regulates cell cycle reentry and
apoptosis of neurons. Mol Biol Cell. 23:3722–3730. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
77
|
Cohen JD, Gard JM, Nagle RB, Dietrich JD,
Monks TJ and Lau SS: ERK crosstalks with 4EBP1 to activate cyclin
D1 translation during quinol-thioether-induced tuberous sclerosis
renal cell carcinoma. Toxicol Sci. 124:75–87. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
78
|
Ravenhall C, Guida E, Harris T, Koutsoubos
V and Stewart A: The importance of ERK activity in the regulation
of cyclin D1 levels and DNA synthesis in human cultured airway
smooth muscle. Br J Pharmacol. 131:17–28. 2000. View Article : Google Scholar : PubMed/NCBI
|
|
79
|
Bortner CD, Hughes FM Jr and Cidlowski JA:
A primary role for K+ and Na+ efflux in the
activation of apoptosis. J Biol Chem. 272:32436–32442. 1997.
View Article : Google Scholar
|
|
80
|
Eggermont J, Trouet D, Carton I and Nilius
B: Cellular function and control of volume-regulated anion
channels. Cell Biochem Biophys. 35:263–274. 2001. View Article : Google Scholar
|
|
81
|
Pedersen SF, Hoffmann EK and Novak I: Cell
volume regulation in epithelial physiology and cancer. Front
Physiol. 4:2332013. View Article : Google Scholar : PubMed/NCBI
|
|
82
|
Stutzin A and Hoffmann EK:
Swelling-activated ion channels: functional regulation in
cell-swelling, proliferation and apoptosis. Acta Physiol (Oxf).
187:27–42. 2006. View Article : Google Scholar
|
|
83
|
Maeno E, Ishizaki Y, Kanaseki T, Hazama A
and Okada Y: Normotonic cell shrinkage because of disordered volume
regulation is an early prerequisite to apoptosis. Proc Natl Acad
Sci USA. 97:9487–9492. 2000. View Article : Google Scholar : PubMed/NCBI
|
|
84
|
Okada Y, Shimizu T, Maeno E, Tanabe S,
Wang X and Takahashi N: Volume-sensitive chloride channels involved
in apoptotic volume decrease and cell death. J Membr Biol.
209:21–29. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
85
|
Qian Y, Du YH, Tang YB, et al: CLC-3
chloride channel prevents apoptosis induced by hydrogen peroxide in
basilar artery smooth muscle cells through mitochondria dependent
pathway. Apoptosis. 16:468–477. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
86
|
Cheng G, Shao Z, Chaudhari B and Agrawal
DK: Involvement of chloride channels in TGF-beta1-induced apoptosis
of human bronchial epithelial cells. Am J Physiol Lung Cell Mol
Physiol. 293:L1339–1347. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
87
|
Zhang HN, Zhou JG, Qiu QY, Ren JL and Guan
YY: CLC-3 chloride channel prevents apoptosis induced by
thapsigargin in PC12 cells. Apoptosis. 11:327–336. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
88
|
Zhang H, Li H, Yang L, et al: The CLC-3
chloride channel associated with microtubules is a target of
paclitaxel in its induced-apoptosis. Sci Rep. 3:26152013.PubMed/NCBI
|
|
89
|
Liu J, Zhang D, Li Y, et al: Discovery of
bufadienolides as a novel class of CLC-3 chloride channel
activators with antitumor activities. J Med Chem. 56:5734–5743.
2013. View Article : Google Scholar : PubMed/NCBI
|
|
90
|
Lin Y, Fukuchi J, Hiipakka RA, Kokontis JM
and Xiang J: Up-regulation of Bcl-2 is required for the progression
of prostate cancer cells from an androgen-dependent to an
androgen-independent growth stage. Cell Res. 17:531–536. 2007.
View Article : Google Scholar : PubMed/NCBI
|
|
91
|
Yang YD, Cho H, Koo JY, et al: TMEM16A
confers receptor-activated calcium-dependent chloride conductance.
Nature. 455:1210–1215. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
92
|
Jin NG, Kim JK, Yang DK, et al:
Fundamental role of CLC-3 in volume-sensitive Cl−
channel function and cell volume regulation in AGS cells. Am J
Physiol Gastrointest Liver Physiol. 285:G938–948. 2003.PubMed/NCBI
|
|
93
|
Gomez-Varela D, Zwick-Wallasch E, Knotgen
H, et al: Monoclonal antibody blockade of the human Eag1 potassium
channel function exerts antitumor activity. Cancer Res.
67:7343–7349. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
94
|
DeBin JA and Strichartz GR: Chloride
channel inhibition by the venom of the scorpion Leiurus
quinquestriatus. Toxicon. 29:1403–1408. 1991. View Article : Google Scholar : PubMed/NCBI
|
|
95
|
Deshane J, Garner CC and Sontheimer H:
Chlorotoxin inhibits glioma cell invasion via matrix
metalloproteinase-2. J Biol Chem. 278:4135–4144. 2003. View Article : Google Scholar
|
|
96
|
Qin C, He B, Dai W, et al: The impact of a
chlorotoxin-modified liposome system on receptor MMP-2 and the
receptor-associated protein CLC-3. Biomaterials. 35:5908–5920.
2014. View Article : Google Scholar : PubMed/NCBI
|
|
97
|
Mamelak AN, Rosenfeld S, Bucholz R, et al:
Phase I single-dose study of intracavitary-administered
iodine-131-TM-601 in adults with recurrent high-grade glioma. J
Clin Oncol. 24:3644–3650. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
98
|
Newman RA, Yang P, Pawlus AD and Block KI:
Cardiac glycosides as novel cancer therapeutic agents. Mol Interv.
8:36–49. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
99
|
Abdel-Rahman MA, Ahmed SH and Nabil ZI: In
vitro cardiotoxicity and mechanism of action of the Egyptian green
toad Bufo viridis skin secretions. Toxicol In Vitro. 24:480–485.
2010. View Article : Google Scholar
|
|
100
|
Barrueto F Jr, Kirrane BM, Cotter BW,
Hoffman RS and Nelson LS: Cardioactive steroid poisoning: a
comparison of plant- and animal-derived compounds. J Med Toxicol.
2:152–155. 2006. View Article : Google Scholar
|
|
101
|
Hu K, Zhu L, Liang H, Hu F and Feng J:
Improved antitumor efficacy and reduced toxicity of liposomes
containing bufadienolides. Arch Pharm Res. 34:1487–1494. 2011.
View Article : Google Scholar : PubMed/NCBI
|
|
102
|
Yoshikawa M, Uchida S, Ezaki J, et al:
CLC-3 deficiency leads to phenotypes similar to human neuronal
ceroid lipofuscinosis. Genes Cells. 7:597–605. 2002. View Article : Google Scholar : PubMed/NCBI
|
