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[1.] Analyse:Hme/Fragment 002 14 - Diskussion
Bearbeitet: 6. November 2014, 14:21 Graf Isolan
Erstellt: 6. November 2014, 14:17 (Graf Isolan)
Fragment, Hme, KomplettPlagiat, SMWFragment, Schulte 2000, Schutzlevel, ZuSichten

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 2, Zeilen: 14-24
Quelle: Schulte 2000
Seite(n): 8, Zeilen: 1-10
1.2.1 Physiological roles of ROMK channels in the kidney

Intracellular K+ (approximately 145 mM) represents the major portion of total body K+. The K+ concentration in the extracellular fluid ranges from 3.5-5 mM. To maintain a constant serum K+ level, 95% of dietary K+ absorbed from the intestine is excreted through the kidney and the remaining portion is eliminated via the colon (Thier, 1986; Stanton, 1989). Under pathophysiological conditions like chronic renal failure, colonic excretion is increased and can contribute significantly to K+ homeostasis (Martin et al., 1986).

K+ secretion in the kidney is a very complex process depending on flow rate, luminal K+, Na+ and Cl- concentrations, hormones and the acid-base status (Stanton, 1989; Wang, 1995; Giebisch, 1998).


Giebisch, G. (1998)
Renal potassium transport: mechanisms and regulation. Am. J. Physiol. 274, F817-F833

Martin, R. S., Panese, S., Virginillo, M., Gimenez, M., Litardo, M., Arrizurieta, E. and Hayslett, J. P. (1986)
Increased secretion of potassium in the rectum of humans with chronic renal failure. Am. J. Kidney Dis. 8, 105-110

Stanton, B. A. (1989)
Renal potassium transport: morphological and functional adaptations. Am. J. Physiol. 257, R989-R997

Thier, S. O. (1986) Potassium physiology. Am. J. Med. 80, 3-7

'Wang, W. H. (1995) View of K+ secretion through the apical K+ [sic] channel of cortical collecting duct. Kidney Int. 48, 1024-1030

1.2.3 Physiological role in the kidney

Intracellular K+ (approximately 145 mM) represents the major portion of total body K+. The K+ concentration in extracellular fluids ranges from 3.5-5 mM. To maintain a constant serum K+ level, 95% of dietary K+ absorbed from the intestine is excreted through the kidney and the remaining portion is eliminated via the colon (Thier, 1986; Stanton, 1989). Under pathophysiological conditions like chronic renal failure, colonic excretion is increased and can contribute significantly to K+ homeostasis (Martin et al., 1986).

K+ secretion in the kidney is a very complex process depending on flow rate, luminal K+, Na+ and Cl- concentrations, hormones and the acid-base status (Stanton, 1989; Wang, 1995; Giebisch, 1998).


Giebisch, G. (1998) Renal potassium transport: mechanism [sic] and regulation. Am. J. Physiol. 274, F817-F833.

Martin, R. S., Panese, S., Virginillo, M., Gimenez, M., Litardo, M., Arrizurieta, E., and Hayslett, J. P. (1986) Increased secretion of potassium in the rectum of humans with chronic renal failure. Am. J. Kidney Dis. 8, 105-110.

Stanton, B. A. (1989) Renal potassium transport: morphological and functional adaptations. Am. J. Physiol. 257, F989-F997.

Thier, S. O. (1986) Potassium physiology. Am. J. Med. 80, 3-7.

Wang, W.-H. (1995) View of K+ secretion through the apical K channel of the [sic] cortical collecting duct. Kidney Int. 48, 1024-1030.

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[1.] Analyse:Hme/Fragment 020 02 - Diskussion
Bearbeitet: 7. November 2014, 01:54 Graf Isolan
Erstellt: 7. November 2014, 01:17 (Graf Isolan)
Fragment, Hme, Jentsch et al 2002, KomplettPlagiat, SMWFragment, Schutzlevel, Unfertig

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Graf Isolan
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Untersuchte Arbeit:
Seite: 20, Zeilen: 2-31
Quelle: Jentsch et al 2002
Seite(n): 524, Zeilen: left col. 35-42.45-53 - right col. 1ff
Renal ClC-K expression is influenced by changes in water and salt load. Dehydration increased transcription of ClC-K1 (Uchida et al., 1993; Vandewalle et al., 1997), compatible with its role in antidiuresis.

ClC-K2 was reported to be overexpressed in the renal medulla of Dahl salt-sensitive rats (Castrop et al., 2000). It was down-regulated by high-salt diet. To understand this regulation, promoters of both isoforms were isolated and subjected to an initial characterization (Uchida et al., 1998, 2000; Rai et al., 1999).

When expressed in Xenopus oocytes, rat ClC-K1 yielded anion currents with a moderate outward rectification that showed only little time-dependent relaxations. Their halide selectivity was Br- > Cl- > I- (Uchida et al., 1998). Currents were decreased by extracellular acidification and by removing extracellular Ca2+ (Uchida et al., 1995). Increasing extracellular Ca2+ concentration led to further enhancement of currents, and no saturation was reached even at 5 mM Ca2+.

Mg2+ and Ba2+ lacked such an effect. To obtain definitive evidence that these currents are mediated by ClC-K1, a valine in a highly conserved domain at the end of D3 was replaced by glutamate, which is found in nearly all other ClC channels at that position. This drastically changed gating, which now slowly opened the channel upon hyperpolarization. Moreover, the halide selectivity was changed to Cl- > Br- > I- (Waldegger and Jentsch, 2000).

ClC-K2 expression was reported to yield similar, outwardly rectified currents, which, however, lacked the initial gating component and displayed a Br- > I- > Cl- selectivity (Adachi et al., 1994). Disconcertingly, a splice variant lacking transmembrane domain D2 gave currents with indistinguishable properties, suggesting that endogenous oocyte currents have been reported.

Two groups (Kieferle et al., 1994; Zimniak et al., 1996) were initially unable to get currents from any ClC-K channel, including both human isoforms. While the expression of ClC-K1 by Uchida and colleagues (1993, 1998) could later be reproduced by Waldegger and Jentsch (Waldegger and Jentsch, 2000), they [remained unable to observe currents with ClC-K2, ClC-Kb, and surprisingly also with ClC-Ka.]


Castrop, H., Kramer, B. K., Riegger, G. A., Kurtz, A. and Wolf, K. (2000)
Overexpression of chloride channel ClC-K2 mRNA in the renal medulla of Dahl salt-sensitive rats. J. Hypertens. 18, 1289-1295

Rai, T., Uchida, S., Sasaki, S. and Marumo, F. (1999)
Isolation and characterization of kidney-specific ClC-K2 chloride channel gene promoter. Biochem. Biophys. Res. Commun. 261, 432-438

Uchida, S., Sasaki, S., Furukawa, T., Hiraoka, M., Imai, T., Hirata, Y. and Marumo, F. (1993)
Molecular cloning of a chloride channel that is regulated by dehydration and expressed predominantly in kidney medulla. J. Biol. Chem. 268, 3821-3824

Uchida, S., Sasaki, S., Nitta, K., Uc hida, K., Horita, S., Nihei, H. and Marumo, F. (1995)
Localization and functional characterization of rat kidney-specific chloride channel, ClC-K1. J. Clin. Invest. 95, 104-113

Uchida, S., Rai, T., Yatsushige, H., Matsumura, Y., Kawasaki, M., Sasaki, S. and Marumo, F. (1998)
Isolation and characterization of kidney-specific ClC-K1 chloride channel gene promoter. Am. J. Physiol. 274, F602-F610

Uchida, S., Tanaka, Y., Ito, H., Saitoh-Ohara, F., Inazawa, J., Yokoyama, K. K., Sasaki, S. and Marumo, F. (2000)
Transcriptional regulation of the ClC-K1 promoter by myc-associated zinc finger protein and kidney-enriched Kruppel-like factor, a novel zinc finger repressor. Mol. Cell. Biol. 20, 7319-7331

Vandewalle, A., Cluzeaud, F., Bens, M., Kieferle, S., Steinmeyer, K. and Jentsch, T. J. (1997)
Localization and induction by dehydration of ClC-K chloride channels in the rat kidney. Am. J. Physiol. 272, F678-F688

Waldegger, S. and Jentsch, T. J. (2000a)
Functional and structural analysis of ClC-K chloride channels involved in renal disease. J. Biol. Chem. 275, 24527-24533

Renal ClC-K expression is influenced by changes in

water and salt load. Dehydration increased transcripts of ClC-K1 (643, 655), compatible with its role in antidiuresis. ClC-K2 was reported to be overexpressed in the renal medulla of Dahl salt-sensitive rats (82). It was downregulated by high-salt diet. To understand this regulation, promoters of both isoforms were isolated and subjected to an initial characterization (508, 642, 645).

2. Functional heterologous expression of ClC-K channels

When expressed in Xenopus oocytes, rat ClC-K1 yielded anion currents with a moderate outward rectification that showed only little time-dependent relaxations (642, 644, 669). Their halide selectivity was Br- > Cl- > I- (642, 669). Currents were decreased by extracellular acidification and by removing extracellular Ca2+ (644, 669). Increasing [Ca2+]o led to further enhancement of currents, and no saturation was reached even at 5 mM Ca2+ (669). Mg2+ and Ba2+ lacked such an effect. To obtain definitive evidence that these currents are mediated by ClC-K1, a valine in a highly conserved domain at the end of D3 (GKVGP) was replaced by glutamate, which is found in nearly all other CLC channels at that position. This drastically changed gating, which now slowly opened the channel upon hyperpolarization. Moreover, the halide selectivity was changed to Cl- > Br- > I- (669).

ClC-K2 expression was reported to yield superficially similar, outwardly rectified currents, which, however, lacked the initial gating component and displayed a Br- > I- > Cl- selectivity (2). Disconcertingly, a splice variant lacking transmembrane domain D2 gave currents with indistinguishable properties (2), suggesting that endogenous oocyte currents have been reported. Two groups (297, 718) were initially unable to get currents from any ClC-K channel, including both human isoforms (297). While the expression of ClC-K1 by Uchida and colleagues (643, 644) could later be reproduced by Waldegger and Jentsch (669), they remained unable to observe currents with ClC-K2, ClC-Kb, and surprisingly also with ClC-Ka, probably the ortholog of ClC-K1.


82. CASTROP H, KRAMER BK, RIEGGER GA, KURTZ A, AND WOLF K. Overexpression of chloride channel CLC-K2 mRNA in the renal medulla of Dahl salt-sensitive rats. J Hypertens 18: 1289–1295, 2000.

508. RAI T, UCHIDA S, SASAKI S, AND MARUMO F. Isolation and characterization of kidney-specific CLC-K2 chloride channel gene promoter. Biochem Biophys Res Commun 261: 432–438, 1999.

642. UCHIDA S, RAI T, YATSUSHIGE H, MATSUMURA Y, KAWASAKI M, SASAKI S, AND MARUMO F. Isolation and characterization of kidney-specific ClC-K1 chloride channel gene promoter. Am J Physiol Renal Physiol 274: F602–F610, 1998.

643. UCHIDA S, SASAKI S, FURUKAWA T, HIRAOKA M, IMAI T, HIRATA Y, AND MARUMO F. Molecular cloning of a chloride channel that is regulated by dehydration and expressed predominantly in kidney. J Biol Chem 268: 3821–3824, 1993.

644. UCHIDA S, SASAKI S, NITTA K, UCHIDA K, HORITA S, NIHEI H, AND MARUMO F. Localization and functional characterization of rat kidney-specific chloride channel, ClC-K1. J Clin Invest 95: 104–113, 1995.

645. UCHIDA S, TANAKA Y, ITO H, SAITOH-OHARA F, INAZAWA J, YOKOYAMA KK, SASAKI S, AND MARUMO F. Transcriptional regulation of the CLC-K1 promoter by myc-associated zinc finger protein and kidney-enriched Kruppel-like factor, a novel zinc finger repressor. Mol Cell Biol 20: 7319–7331, 2000.

655. VANDEWALLE A, CLUZEAUD F, BENS M, KIEFERLE S, STEINMEYER K, AND JENTSCH TJ. Localization and induction by dehydration of ClC-K chloride channels in the rat kidney. Am J Physiol Renal Physiol 272: F678–F688, 1997.

669. WALDEGGER S AND JENTSCH TJ. Functional and structural analysis of ClC-K chloride channels involved in renal disease. J Biol Chem 275: 24527–24533, 2000.

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