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Artikel ; Online: Scn1a

Yamagata, Tetsushi / Ogiwara, Ikuo / Tatsukawa, Tetsuya / Suzuki, Toshimitsu / Otsuka, Yuka / Imaeda, Nao / Mazaki, Emi / Inoue, Ikuyo / Tokonami, Natsuko / Hibi, Yurina / Itohara, Shigeyoshi / Yamakawa, Kazuhiro

eLife

2023 Band 12

Abstract: Expressions of voltage-gated sodium channels Nav1.1 and Nav1.2, encoded ... ...

Abstract	Expressions of voltage-gated sodium channels Nav1.1 and Nav1.2, encoded by
Mesh-Begriff(e)	Mice ; Animals ; Mice, Transgenic ; Neocortex/metabolism ; Green Fluorescent Proteins/metabolism ; Pyramidal Tracts ; NAV1.1 Voltage-Gated Sodium Channel/genetics ; Neurons/physiology ; Pyramidal Cells/metabolism
Chemische Substanzen	Green Fluorescent Proteins (147336-22-9) ; NAV1.1 Voltage-Gated Sodium Channel ; Scn1a protein, mouse
Sprache	Englisch
Erscheinungsdatum	2023-05-23
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.87495
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The excretion of uromodulin is modulated by the calcium-sensing receptor.

Tokonami, Natsuko / Olinger, Eric / Debaix, Huguette / Houillier, Pascal / Devuyst, Olivier

Kidney international

2018 Band 94, Heft 5, Seite(n) 882–886

Abstract: Uromodulin is produced in the thick ascending limb, but little is known about regulation of its excretion in urine. Using mouse and cellular models, we demonstrate that excretion of uromodulin by thick ascending limb cells is increased or decreased upon ... ...

Abstract	Uromodulin is produced in the thick ascending limb, but little is known about regulation of its excretion in urine. Using mouse and cellular models, we demonstrate that excretion of uromodulin by thick ascending limb cells is increased or decreased upon inactivation or activation of the calcium-sensing receptor (CaSR), respectively. These effects reflect changes in uromodulin trafficking and likely involve alterations in intracellular cyclic adenosine monophosphate (cAMP) levels. Administration of the CaSR agonist cinacalcet led to a rapid reduction of urinary uromodulin excretion in healthy subjects. Modulation of uromodulin excretion by the CaSR may be clinically relevant considering the increasing use of CaSR modulators.
Mesh-Begriff(e)	Animals ; Calcium/metabolism ; Cyclic AMP/analysis ; Loop of Henle/metabolism ; Mice ; Receptors, Calcium-Sensing/genetics ; Receptors, Calcium-Sensing/physiology ; Uromodulin/urine
Chemische Substanzen	Receptors, Calcium-Sensing ; Uromodulin ; Cyclic AMP (E0399OZS9N) ; Calcium (SY7Q814VUP)
Sprache	Englisch
Erscheinungsdatum	2018-11-15
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2018.07.022
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Endothelin-1 mediates natriuresis but not polyuria during vitamin D-induced acute hypercalcaemia.

Tokonami, Natsuko / Cheval, Lydie / Monnay, Isabelle / Meurice, Guillaume / Loffing, Johannes / Feraille, Eric / Houillier, Pascal

The Journal of physiology

2017 Band 595, Heft 8, Seite(n) 2535–2550

Abstract: Key points: Hypercalcaemia can occur under various pathological conditions, such as primary hyperparathyroidism, malignancy or granulomatosis, and it induces natriuresis and polyuria in various species via an unknown mechanism. A previous study ... ...

Abstract	Key points: Hypercalcaemia can occur under various pathological conditions, such as primary hyperparathyroidism, malignancy or granulomatosis, and it induces natriuresis and polyuria in various species via an unknown mechanism. A previous study demonstrated that hypercalcaemia induced by vitamin D in rats increased endothelin (ET)-1 expression in the distal nephron, which suggests the involvement of the ET system in hypercalcaemia-induced effects. In the present study, we demonstrate that, during vitamin D-induced hypercalcaemia, the activation of ET system by increased ET-1 is responsible for natriuresis but not for polyuria. Vitamin D-treated hypercalcaemic mice showed a blunted response to amiloride, suggesting that epithelial sodium channel function is inhibited. We have identified an original pathway that specifically mediates the effects of vitamin D-induced hypercalcaemia on sodium handling in the distal nephron without affecting water handling. Abstract: Acute hypercalcaemia increases urinary sodium and water excretion; however, the underlying molecular mechanism remains unclear. Because vitamin D-induced hypercalcaemia increases the renal expression of endothelin (ET)-1, we hypothesized that ET-1 mediates the effects of hypercalcaemia on renal sodium and water handling. Hypercalcaemia was induced in 8-week-old, parathyroid hormone-supplemented, male mice by oral administration of dihydrotachysterol (DHT) for 3 days. DHT-treated mice became hypercalcaemic and displayed increased urinary water and sodium excretion compared to controls. mRNA levels of ET-1 and the transcription factors CCAAT-enhancer binding protein β and δ were specifically increased in the distal convoluted tubule and downstream segments in DHT-treated mice. To examine the role of the ET system in hypercalcaemia-induced natriuresis and polyuria, mice were treated with the ET-1 receptor antagonist macitentan, with or without DHT. Mice treated with both macitentan and DHT displayed hypercalcaemia and polyuria similar to that in mice treated with DHT alone; however, no increase in urinary sodium excretion was observed. To identify the affected sodium transport mechanism, we assessed the response to various diuretics in control and DHT-treated hypercalcaemic mice. Amiloride, an inhibitor of the epithelial sodium channel (ENaC), increased sodium excretion to a lesser extent in DHT-treated mice compared to control mice. Mice treated with either macitentan+DHT or macitentan alone had a similar response to amiloride. In summary, vitamin D-induced hypercalcaemia increases the renal production of ET-1 and decreases ENaC activity, which is probably responsible for the rise in urinary sodium excretion but not for polyuria.
Mesh-Begriff(e)	Acute Disease ; Animals ; Cell Line, Transformed ; Endothelin-1/physiology ; Hypercalcemia/chemically induced ; Hypercalcemia/metabolism ; Hypercalcemia/urine ; Kidney Tubules/drug effects ; Kidney Tubules/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Natriuresis/drug effects ; Natriuresis/physiology ; Polyuria/metabolism ; Polyuria/urine ; Vitamin D/toxicity
Chemische Substanzen	Endothelin-1 ; Vitamin D (1406-16-2)
Sprache	Englisch
Erscheinungsdatum	2017-03-23
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP273610
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Uromodulin is expressed in the distal convoluted tubule, where it is critical for regulation of the sodium chloride cotransporter NCC.

Tokonami, Natsuko / Takata, Tomoaki / Beyeler, Jan / Ehrbar, Iris / Yoshifuji, Ayumi / Christensen, Erik I / Loffing, Johannes / Devuyst, Olivier / Olinger, Eric G

Kidney international

2018 Band 94, Heft 4, Seite(n) 701–715

Abstract: Uromodulin, the most abundant protein in normal urine, is essentially produced by the cells lining the thick ascending limb. There it regulates the activity of the cotransporter NKCC2 and is involved in sodium chloride handling and blood pressure ... ...

Abstract	Uromodulin, the most abundant protein in normal urine, is essentially produced by the cells lining the thick ascending limb. There it regulates the activity of the cotransporter NKCC2 and is involved in sodium chloride handling and blood pressure regulation. Conflicting reports suggested that uromodulin may also be expressed in the distal convoluted tubule (DCT) where its role remains unknown. Using microdissection studies combined with fluorescent in situ hybridization and co-immunostaining analyses, we found a significant expression of uromodulin in mouse and human DCT at approximately 10% of thick ascending limb expression levels, but restricted to the early part of the DCT (DCT1). Genetic deletion of Umod in mouse was reflected by a major shift in NCC activity from the DCT1 to the downstream DCT2 segment, paralleled by a compensatory expansion of DCT2. By increasing the distal sodium chloride and calcium ion load with chronic furosemide administration, an intrinsic compensatory defect in the DCT from Umod
Mesh-Begriff(e)	Animals ; Furosemide/pharmacology ; Gene Expression ; HEK293 Cells ; Humans ; Hypercalciuria/chemically induced ; Hypercalciuria/genetics ; Kidney Tubules, Distal/metabolism ; Kidney Tubules, Distal/physiology ; Male ; Mice ; Mice, Knockout ; Phosphorylation ; RNA, Messenger ; Sodium/metabolism ; Sodium Potassium Chloride Symporter Inhibitors/pharmacology ; Solute Carrier Family 12, Member 1/antagonists & inhibitors ; Solute Carrier Family 12, Member 1/genetics ; Solute Carrier Family 12, Member 1/metabolism ; Uromodulin/biosynthesis ; Uromodulin/genetics ; Uromodulin/metabolism
Chemische Substanzen	RNA, Messenger ; SLC12A1 protein, human ; Slc12a1 protein, mouse ; Sodium Potassium Chloride Symporter Inhibitors ; Solute Carrier Family 12, Member 1 ; UMOD protein, human ; Umod protein, mouse ; Uromodulin ; Furosemide (7LXU5N7ZO5) ; Sodium (9NEZ333N27)
Sprache	Englisch
Erscheinungsdatum	2018-07-12
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2018.04.021
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Role of the renal circadian timing system in maintaining water and electrolytes homeostasis.

Firsov, Dmitri / Tokonami, Natsuko / Bonny, Olivier

Molecular and cellular endocrinology

2012 Band 349, Heft 1, Seite(n) 51–55

Abstract: Many basic physiological functions exhibit circadian rhythmicity. These functional rhythms are driven, in part, by the circadian clock, an ubiquitous molecular mechanism allowing cells and tissues to anticipate regular environmental events and to prepare ...

Abstract	Many basic physiological functions exhibit circadian rhythmicity. These functional rhythms are driven, in part, by the circadian clock, an ubiquitous molecular mechanism allowing cells and tissues to anticipate regular environmental events and to prepare for them. This mechanism has been shown to play a particularly important role in maintaining stability (homeostasis) of internal conditions. Because the homeostatic equilibrium is continuously challenged by environmental changes, the role of the circadian clock is thought to consist in the anticipative adjustment of homeostatic pathways in relation with the 24h environmental cycle. The kidney is the principal organ responsible for the regulation of the composition and volume of extracellular fluids (ECF). Several major parameters of kidney function, including renal plasma flow (RPF), glomerular filtration rate (GFR) and tubular reabsorption and secretion have been shown to exhibit strong circadian oscillations. Recent evidence suggest that the circadian clock can be involved in generation of these rhythms through external circadian time cues (e.g. humoral factors, activity and body temperature rhythms) or, trough the intrinsic renal circadian clock. Here, we discuss the role of renal circadian mechanisms in maintaining homeostasis of water and three major ions, namely, Na(+), K(+) and Cl(-).
Mesh-Begriff(e)	Animals ; Chlorides/metabolism ; Circadian Clocks ; Circadian Rhythm ; Homeostasis ; Hormones/metabolism ; Humans ; Kidney/metabolism ; Kidney/physiology ; Potassium/metabolism ; Sodium/metabolism ; Water/metabolism ; Water-Electrolyte Balance
Chemische Substanzen	Chlorides ; Hormones ; Water (059QF0KO0R) ; Sodium (9NEZ333N27) ; Potassium (RWP5GA015D)
Sprache	Englisch
Erscheinungsdatum	2012-02-05
Erscheinungsland	Ireland
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2011.06.037
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Author Correction: Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency.

Nature communications

2020 Band 11, Heft 1, Seite(n) 1719

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

Abstract	An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Sprache	Englisch
Erscheinungsdatum	2020-04-01
Erscheinungsland	England
Dokumenttyp	Published Erratum
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-15565-6
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Hepsin-mediated Processing of Uromodulin is Crucial for Salt-sensitivity and Thick Ascending Limb Homeostasis.

Olinger, Eric / Lake, Jennifer / Sheehan, Susan / Schiano, Guglielmo / Takata, Tomoaki / Tokonami, Natsuko / Debaix, Huguette / Consolato, Francesco / Rampoldi, Luca / Korstanje, Ron / Devuyst, Olivier

Scientific reports

2019 Band 9, Heft 1, Seite(n) 12287

Abstract: Uromodulin is a zona pellucida-type protein essentially produced in the thick ascending limb (TAL) of the mammalian kidney. It is the most abundant protein in normal urine. Defective uromodulin processing is associated with various kidney disorders. The ... ...

Abstract	Uromodulin is a zona pellucida-type protein essentially produced in the thick ascending limb (TAL) of the mammalian kidney. It is the most abundant protein in normal urine. Defective uromodulin processing is associated with various kidney disorders. The luminal release and subsequent polymerization of uromodulin depend on its cleavage mediated by the serine protease hepsin. The biological relevance of a proper cleavage of uromodulin remains unknown. Here we combined in vivo testing on hepsin-deficient mice, ex vivo analyses on isolated tubules and in vitro studies on TAL cells to demonstrate that hepsin influence on uromodulin processing is an important modulator of salt transport via the sodium cotransporter NKCC2 in the TAL. At baseline, hepsin-deficient mice accumulate uromodulin, along with hyperactivated NKCC2, resulting in a positive sodium balance and a better adaptation to water deprivation. In conditions of high salt intake, defective uromodulin processing predisposes hepsin-deficient mice to a salt-wasting phenotype, with a decreased salt sensitivity. These modifications are associated with intracellular accumulation of uromodulin, endoplasmic reticulum-stress and signs of tubular damage. These studies expand the physiological role of hepsin and uromodulin and highlight the importance of hepsin-mediated processing of uromodulin for kidney tubule homeostasis and salt sensitivity.
Mesh-Begriff(e)	Animals ; Base Sequence ; Cell Line ; Homeostasis/drug effects ; Kidney Tubules/drug effects ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Mice, Inbred C57BL ; Mutation/genetics ; Phenotype ; Serine Endopeptidases/genetics ; Serine Endopeptidases/metabolism ; Sodium Chloride/pharmacology ; Solute Carrier Family 12, Member 1/metabolism ; Uromodulin/metabolism ; Uromodulin/urine
Chemische Substanzen	Solute Carrier Family 12, Member 1 ; Uromodulin ; Sodium Chloride (451W47IQ8X) ; Serine Endopeptidases (EC 3.4.21.-) ; hepsin (EC 3.4.21.-)
Sprache	Englisch
Erscheinungsdatum	2019-08-23
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, American Recovery and Reinvestment Act ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-48300-3
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Hepsin-mediated Processing of Uromodulin is Crucial for Salt-sensitivity and Thick Ascending Limb Homeostasis

Eric Olinger / Jennifer Lake / Susan Sheehan / Guglielmo Schiano / Tomoaki Takata / Natsuko Tokonami / Huguette Debaix / Francesco Consolato / Luca Rampoldi / Ron Korstanje / Olivier Devuyst

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Band 15

Abstract: Abstract Uromodulin is a zona pellucida-type protein essentially produced in the thick ascending limb (TAL) of the mammalian kidney. It is the most abundant protein in normal urine. Defective uromodulin processing is associated with various kidney ... ...

Abstract	Abstract Uromodulin is a zona pellucida-type protein essentially produced in the thick ascending limb (TAL) of the mammalian kidney. It is the most abundant protein in normal urine. Defective uromodulin processing is associated with various kidney disorders. The luminal release and subsequent polymerization of uromodulin depend on its cleavage mediated by the serine protease hepsin. The biological relevance of a proper cleavage of uromodulin remains unknown. Here we combined in vivo testing on hepsin-deficient mice, ex vivo analyses on isolated tubules and in vitro studies on TAL cells to demonstrate that hepsin influence on uromodulin processing is an important modulator of salt transport via the sodium cotransporter NKCC2 in the TAL. At baseline, hepsin-deficient mice accumulate uromodulin, along with hyperactivated NKCC2, resulting in a positive sodium balance and a better adaptation to water deprivation. In conditions of high salt intake, defective uromodulin processing predisposes hepsin-deficient mice to a salt-wasting phenotype, with a decreased salt sensitivity. These modifications are associated with intracellular accumulation of uromodulin, endoplasmic reticulum-stress and signs of tubular damage. These studies expand the physiological role of hepsin and uromodulin and highlight the importance of hepsin-mediated processing of uromodulin for kidney tubule homeostasis and salt sensitivity.
Schlagwörter	Medicine ; R ; Science ; Q
Thema/Rubrik (Code)	570
Sprache	Englisch
Erscheinungsdatum	2019-08-01T00:00:00Z
Verlag	Nature Publishing Group
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel: Role of the renal circadian timing system in maintaining water and electrolytes homeostasis

Firsov, Dmitri / Tokonami, Natsuko / Bonny, Olivier

Molecular and cellular endocrinology. 2012 Feb. 5, v. 349, no. 1

2012

Abstract	Many basic physiological functions exhibit circadian rhythmicity. These functional rhythms are driven, in part, by the circadian clock, an ubiquitous molecular mechanism allowing cells and tissues to anticipate regular environmental events and to prepare for them. This mechanism has been shown to play a particularly important role in maintaining stability (homeostasis) of internal conditions. Because the homeostatic equilibrium is continuously challenged by environmental changes, the role of the circadian clock is thought to consist in the anticipative adjustment of homeostatic pathways in relation with the 24h environmental cycle. The kidney is the principal organ responsible for the regulation of the composition and volume of extracellular fluids (ECF). Several major parameters of kidney function, including renal plasma flow (RPF), glomerular filtration rate (GFR) and tubular reabsorption and secretion have been shown to exhibit strong circadian oscillations. Recent evidence suggest that the circadian clock can be involved in generation of these rhythms through external circadian time cues (e.g. humoral factors, activity and body temperature rhythms) or, trough the intrinsic renal circadian clock. Here, we discuss the role of renal circadian mechanisms in maintaining homeostasis of water and three major ions, namely, Na⁺, K⁺ and Cl⁻.
Schlagwörter	body temperature ; chlorides ; circadian rhythm ; electrolytes ; extracellular fluids ; glomerular filtration rate ; homeostasis ; ions ; kidneys ; potassium ; secretion ; sodium ; tissues
Sprache	Englisch
Erscheinungsverlauf	2012-0205
Umfang	p. 51-55.
Erscheinungsort	Elsevier Ireland Ltd
Dokumenttyp	Artikel
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2011.06.037
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Author Correction

Nature Communications, Vol 11, Iss 1, Pp 1-

Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiency

2020 Band 1

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

Abstract	An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Schlagwörter	Science ; Q
Sprache	Englisch
Erscheinungsdatum	2020-04-01T00:00:00Z
Verlag	Nature Publishing Group
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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