Paracellin-1 - Revision history

Nnjm2 at 07:16, 24 August 2011

2011-08-24T07:16:13Z

← Older revision		Revision as of 07:16, 24 August 2011
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	'''<u>Mutation of Paracellin-1</u>'''		'''<u>Mutation of Paracellin-1</u>'''

	Recessive mutations in Paracellin-1 leads to [[Hypomagnesaemia\|hypomagnesaemia]] in humans.  [[Magnesium\|Magnesium]] movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less [[Magnesium\|magnesium]] being reabsorbed.  [[Calcium\|Calcium]] movement is also disturbed causing [[Hypercalciuria\|hypercalciuria]] and [[Nephrocalcinosis\|nephrocalcinosis]] <ref>Hampson G, Konrad MA, Scoble J. (2008) Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): compound heterozygous mutation in the claudin 16 (CLDN16) gene. BMC nephrology Journal. 9:12</ref>.		[[Recessive_gene\|Recessive]] mutations in Paracellin-1 leads to [[Hypomagnesaemia\|hypomagnesaemia]] in humans.  [[Magnesium\|Magnesium]] movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less [[Magnesium\|magnesium]] being reabsorbed.  [[Calcium\|Calcium]] movement is also disturbed causing [[Hypercalciuria\|hypercalciuria]] and [[Nephrocalcinosis\|nephrocalcinosis]] <ref>Hampson G, Konrad MA, Scoble J. (2008) Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): compound heterozygous mutation in the claudin 16 (CLDN16) gene. BMC nephrology Journal. 9:12</ref>.

	=== References ===		=== References ===

	<references /><br>		<references /><br>

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Nnjm2 at 14:41, 14 November 2010

2010-11-14T14:41:38Z

← Older revision		Revision as of 14:41, 14 November 2010
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	Paracellin-1, also known as Claudin 16, is one of the transmembrane linker proteins of tight junctions and is part of the Claudin family.  This protein is found in the thick ascending limb of the [[Loop of Henle\|Loop of Henle]] in the Renal Tubule [2].		Paracellin-1, also known as Claudin 16, is one of the [[Transmembrane\|transmembrane]] linker [[Proteins\|proteins]] of [[Tight junctions\|tight junctions]] and is part of the Claudin family.  This [[Proteins\|protein]] is found in the thick ascending limb of the [[Loop of Henle\|Loop of Henle]] in the [[Renal Tubule\|Renal Tubule]] <ref>Ikari A, Ito M, Okude C, Sawada H, Harada H, Degawa M, Sakai H, Takahashi T, Sugatani J, Miwa M. (2008) Claudin-16 is directly phosphorylated by protein kinase A independently of a vasodilator-stimulated phosphoprotein-mediated pathway. Journal of cellular physiology. 214(1):221-9.</ref>.

	'''<u>Mutation of Paracellin-1</u>'''		'''<u>Mutation of Paracellin-1</u>'''

	Recessive mutations in Paracellin-1 leads to hypomagnesaemia in humans.  Magnesium movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less magnesium being reabsorbed.  Calcium movement is also disturbed causing hypercalciuria and nephrocalcinosis [1].		Recessive mutations in Paracellin-1 leads to [[Hypomagnesaemia\|hypomagnesaemia]] in humans.  [[Magnesium\|Magnesium]] movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less [[Magnesium\|magnesium]] being reabsorbed.  [[Calcium\|Calcium]] movement is also disturbed causing [[Hypercalciuria\|hypercalciuria]] and [[Nephrocalcinosis\|nephrocalcinosis]] <ref>Hampson G, Konrad MA, Scoble J. (2008) Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): compound heterozygous mutation in the claudin 16 (CLDN16) gene. BMC nephrology Journal. 9:12</ref>.

	~~<u>'''~~References~~'''</u>~~		=== References ===

	1. Hampson G, Konrad MA, Scoble J. (2008) Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): compound heterozygous mutation in the claudin 16 (CLDN16) gene. BMC nephrology Journal. 9:12.		<references /><br>

	2. Ikari A, Ito M, Okude C, Sawada H, Harada H, Degawa M, Sakai H, Takahashi T, Sugatani J, Miwa M. (2008) Claudin-16 is directly phosphorylated by protein kinase A independently of a vasodilator-stimulated phosphoprotein-mediated pathway. Journal of cellular physiology. 214(1):221-9.		<br>

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104645695 at 13:42, 14 November 2010

2010-11-14T13:42:57Z

← Older revision		Revision as of 13:42, 14 November 2010
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	Paracellin-1, also known as Claudin 16, is one of the transmembrane linker proteins of tight junctions and is part of the Claudin family.  This protein is found in the thick ascending limb of the [[Loop of Henle\|Loop of Henle]] in the Renal Tubule.		Paracellin-1, also known as Claudin 16, is one of the transmembrane linker proteins of tight junctions and is part of the Claudin family.  This protein is found in the thick ascending limb of the [[Loop of Henle\|Loop of Henle]] in the Renal Tubule [2].

	'''<u>Mutation of Paracellin-1</u>'''		'''<u>Mutation of Paracellin-1</u>'''

	Recessive mutations in Paracellin-1 leads to hypomagnesaemia in humans.  Magnesium movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less magnesium being reabsorbed.  Calcium movement is also disturbed causing hypercalciuria and nephrocalcinosis.		Recessive mutations in Paracellin-1 leads to hypomagnesaemia in humans.  Magnesium movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less magnesium being reabsorbed.  Calcium movement is also disturbed causing hypercalciuria and nephrocalcinosis [1].

	<u>'''References'''</u>		<u>'''References'''</u>

	Hampson G, Konrad MA, Scoble J. (2008) Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): compound heterozygous mutation in the claudin 16 (CLDN16) gene. BMC nephrology Journal. 9:12.		1. Hampson G, Konrad MA, Scoble J. (2008) Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): compound heterozygous mutation in the claudin 16 (CLDN16) gene. BMC nephrology Journal. 9:12.

	Ikari A, Ito M, Okude C, Sawada H, Harada H, Degawa M, Sakai H, Takahashi T, Sugatani J, Miwa M. (2008) Claudin-16 is directly phosphorylated by protein kinase A independently of a vasodilator-stimulated phosphoprotein-mediated pathway. Journal of cellular physiology. 214(1):221-9.

			2. Ikari A, Ito M, Okude C, Sawada H, Harada H, Degawa M, Sakai H, Takahashi T, Sugatani J, Miwa M. (2008) Claudin-16 is directly phosphorylated by protein kinase A independently of a vasodilator-stimulated phosphoprotein-mediated pathway. Journal of cellular physiology. 214(1):221-9.

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104645695 at 13:40, 14 November 2010

2010-11-14T13:40:47Z

← Older revision		Revision as of 13:40, 14 November 2010
Line 3:		Line 3:
	'''<u>Mutation of Paracellin-1</u>'''		'''<u>Mutation of Paracellin-1</u>'''

	Recessive mutations in Paracellin-1 leads to hypomagnesaemia in humans.  Magnesium movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less magnesium being reabsorbed.  Calcium movement is also disturbed causing ~~hypocalcaemia~~.		Recessive mutations in Paracellin-1 leads to hypomagnesaemia in humans.  Magnesium movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less magnesium being reabsorbed.  Calcium movement is also disturbed causing hypercalciuria and nephrocalcinosis.

			<u>'''References'''</u>

			Hampson G, Konrad MA, Scoble J. (2008) Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): compound heterozygous mutation in the claudin 16 (CLDN16) gene. BMC nephrology Journal. 9:12.

			Ikari A, Ito M, Okude C, Sawada H, Harada H, Degawa M, Sakai H, Takahashi T, Sugatani J, Miwa M. (2008) Claudin-16 is directly phosphorylated by protein kinase A independently of a vasodilator-stimulated phosphoprotein-mediated pathway. Journal of cellular physiology. 214(1):221-9.



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104645695 at 22:25, 9 November 2010

2010-11-09T22:25:38Z

← Older revision		Revision as of 22:25, 9 November 2010
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	Paracellin-1, also known as Claudin 16, is one of the transmembrane linker proteins of tight junctions and is part of the Claudin family.  This protein is ~~only~~ found in the thick ascending limb of the [[Loop of Henle\|Loop of Henle]] in the Renal Tubule.		Paracellin-1, also known as Claudin 16, is one of the transmembrane linker proteins of tight junctions and is part of the Claudin family.  This protein is found in the thick ascending limb of the [[Loop of Henle\|Loop of Henle]] in the Renal Tubule.

	'''<u>Mutation of Paracellin-1</u>'''		'''<u>Mutation of Paracellin-1</u>'''

	Recessive mutations in Paracellin-1 leads to hypomagnesaemia in humans.  Magnesium movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less magnesium being reabsorbed.  Calcium movement is also disturbed causing hypocalcaemia.		Recessive mutations in Paracellin-1 leads to hypomagnesaemia in humans.  Magnesium movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less magnesium being reabsorbed.  Calcium movement is also disturbed causing hypocalcaemia.

104645695: Created page with 'Paracellin-1, also known as Claudin 16, is one of the transmembrane linker proteins of tight junctions and is part of the Claudin family. This protein is only found in the …'

2010-11-09T22:24:15Z

Created page with 'Paracellin-1, also known as Claudin 16, is one of the transmembrane linker proteins of tight junctions and is part of the Claudin family. This protein is only found in the …'

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Paracellin-1, also known as Claudin 16, is one of the transmembrane linker proteins of tight junctions and is part of the Claudin family.  This protein is only found in the thick ascending limb of the [[Loop of Henle|Loop of Henle]] in the Renal Tubule. 

'''<u>Mutation of Paracellin-1</u>'''

Recessive mutations in Paracellin-1 leads to hypomagnesaemia in humans.  Magnesium movement in the thick ascending limb is controlled by a paracellular pathway which is altered by mutations in Paracellin-1 which therefore leads to less magnesium being reabsorbed.  Calcium movement is also disturbed causing hypocalcaemia.