User:Anat Levit/Sandbox 1: Difference between revisions

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The prokineticin receptors have been found to be involved in various pathologies involving the cardiovascular, reproductive, endocrine and nervous systems. Notably, PROKR2 has been found to be <scene name='User:Anat_Levit/Sandbox_1/Pkr1_ks_mutations/1'>mutated in Kallmann syndrome</scene> with dilated cardiomyopathy, a hypogonadism caused by a deficiency of gonadotropin-releasing hormone (GnRH) (see Wikipedia:

[http://en.wikipedia.org/wiki/Kallmann_syndrome Kallmann syndrome]). Except for V331M and R357W which are Leu and Asn in PROKR1, respectively, all other residues mutated in PROKR2 are identical in PROKR1. Interestingly, two of the mutated residues, W178 (4.50) and P290 (6.50), are two of the most conserved residues in family A GPCRs (<scene name='User:Anat_Levit/Sandbox_1/Pkr_colored_by_homology/4'>restore initial scene</scene>).

[http://en.wikipedia.org/wiki/Kallmann_syndrome Kallmann syndrome]). Except for V331M and R357W (colored red) which are Leu and Asn in PROKR1, respectively, all other residues mutated in PROKR2 are identical in PROKR1 (colored blue). Interestingly, two of the mutated residues, W178 (4.50) and P290 (6.50), are two of the most conserved residues in family A GPCRs (<scene name='User:Anat_Levit/Sandbox_1/Pkr_colored_by_homology/4'>restore initial scene</scene>).

[[Image:ColorKey_ConSurf_NoYellow_NoGray.gif|right|200 px]]

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 The prokineticin receptors have been found to be involved in various pathologies involving the cardiovascular, reproductive, endocrine and nervous systems. Notably, PROKR2 has been found to be <scene name='User:Anat_Levit/Sandbox_1/Pkr1_ks_mutations/1'>mutated in Kallmann syndrome</scene> with dilated cardiomyopathy, a hypogonadism caused by a deficiency of gonadotropin-releasing hormone (GnRH) (see Wikipedia:
-[http://en.wikipedia.org/wiki/Kallmann_syndrome Kallmann syndrome]). Except for V331M and R357W which are Leu and Asn in PROKR1, respectively, all other residues mutated in PROKR2 are identical in PROKR1. Interestingly, two of the mutated residues, W178 (4.50) and P290 (6.50), are two of the most conserved residues in family A GPCRs (<scene name='User:Anat_Levit/Sandbox_1/Pkr_colored_by_homology/4'>restore initial scene</scene>).
+[http://en.wikipedia.org/wiki/Kallmann_syndrome Kallmann syndrome]). Except for V331M and R357W (colored red) which are Leu and Asn in PROKR1, respectively, all other residues mutated in PROKR2 are identical in PROKR1 (colored blue). Interestingly, two of the mutated residues, W178 (4.50) and P290 (6.50), are two of the most conserved residues in family A GPCRs (<scene name='User:Anat_Levit/Sandbox_1/Pkr_colored_by_homology/4'>restore initial scene</scene>).
 [[Image:ColorKey_ConSurf_NoYellow_NoGray.gif|right|200 px]]