1fil: Difference between revisions

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~~[[Image:1fil.png|left|200px]]~~

===HUMAN PLATELET PROFILIN I CRYSTALLIZED IN HIGH SALT ACTIN-BINDING PROTEIN===

===~~HUMAN PLATELET PROFILIN I CRYSTALLIZED IN HIGH SALT ACTIN~~-~~BINDING PROTEIN===~~

==Disease==

[[http://www.uniprot.org/uniprot/PROF1_HUMAN PROF1_HUMAN]] Defects in PFN1 are the cause of amyotrophic lateral sclerosis 18 (ALS18) [MIM:[http://omim.org/entry/614808 614808]]. A neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases.<ref>PMID:22801503</ref>

~~{{ABSTRACT_PUBMED_014695246}}~~

==Function==

[[http://www.uniprot.org/uniprot/PROF1_HUMAN PROF1_HUMAN]] Binds to actin and affects the structure of the cytoskeleton. At high concentrations, profilin prevents the polymerization of actin, whereas it enhances it at low concentrations. By binding to PIP2, it inhibits the formation of IP3 and DG. Inhibits androgen receptor (AR) and HTT aggregation and binding of G-actin is essential for its inhibition of AR.<ref>PMID:18573880</ref>

==About this Structure==

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==Reference==

[[Category: Homo sapiens]]

[[Category: Almo, S C.]]

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@@ Line 1: / Line 1: @@
-[[Image:1fil.png|left|200px]]
 {{STRUCTURE_1fil|  PDB=1fil  |  SCENE=  }}
+===HUMAN PLATELET PROFILIN I CRYSTALLIZED IN HIGH SALT ACTIN-BINDING PROTEIN===
+{{ABSTRACT_PUBMED_014695246}}
-===HUMAN PLATELET PROFILIN I CRYSTALLIZED IN HIGH SALT ACTIN-BINDING PROTEIN===
+==Disease==
+[[http://www.uniprot.org/uniprot/PROF1_HUMAN PROF1_HUMAN]] Defects in PFN1 are the cause of amyotrophic lateral sclerosis 18 (ALS18) [MIM:[http://omim.org/entry/614808 614808]]. A neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases.<ref>PMID:22801503</ref>
-{{ABSTRACT_PUBMED_014695246}}
+==Function==
+[[http://www.uniprot.org/uniprot/PROF1_HUMAN PROF1_HUMAN]] Binds to actin and affects the structure of the cytoskeleton. At high concentrations, profilin prevents the polymerization of actin, whereas it enhances it at low concentrations. By binding to PIP2, it inhibits the formation of IP3 and DG. Inhibits androgen receptor (AR) and HTT aggregation and binding of G-actin is essential for its inhibition of AR.<ref>PMID:18573880</ref>
 ==About this Structure==
@@ Line 11: / Line 13: @@
 ==Reference==
-<ref group="xtra">PMID:014695246</ref><ref group="xtra">PMID:017154716</ref><references group="xtra"/>
+<ref group="xtra">PMID:014695246</ref><ref group="xtra">PMID:017154716</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Almo, S C.]]