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Literature summary for 2.7.1.153 extracted from

  • Runyan, C.E.; Liu, Z.; Schnaper, H.W.
    Phosphatidylinositol 3-kinase and Rab5 GTPase inversely regulate the Smad anchor for receptor activation (SARA) protein independently of transforming growth factor-beta1 (2012), J. Biol. Chem., 287, 35815-35824.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens P27986 regulatory subunit alpha
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Source Tissue

Source Tissue Comment Organism Textmining
epithelial cell renal proximal tubule epithelial cell Homo sapiens
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kidney renal proximal tubule epithelial cell Homo sapiens
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General Information

General Information Comment Organism
physiological function phosphatidylinositol 3-kinase pathway inhibition is sufficient to reduce expression of Smad anchor for receptor activation protein, i.e. SARA. Phosphatidylinositol 3-kinase-dependent depletion of SARA is apparent within 6 h and does not occur at the mRNA or promoter level but is blocked by inhibition of proteasome-mediated degradation. It is a direct effect of phosphatidylinositol 3-kinase subunit alpha action, and coimmunoprecipitation of SARA and subunit alpha confirm that these proteins interact. Expression of GTPase-deficient Rab5 leads to endosomal enlargement and reduced SARA protein expression, similar to that seen with phosphatidylinositol 3-kinase inhibition Homo sapiens