Identification of the Novel Interacting Partners of the Mammalian Target of Rapamycin Complex 1 in Human CCRF-CEM and HEK293 Cells.
Göttingen, Germany. In Int J Mol Sci, Dec 2013
These new mTORC1 interacting partners include heterogeneous nuclear ribonucleoproteins A2/B1, enhancer of mRNA decapping protein 4, 60S acidic ribosomal protein, P0, nucleolin, dynamin 2, glyceraldehyde 3 phosphate dehydrogenase, 2-oxoglutarate dehydrogenase, glycosyl transferase 25 family member 1 and prohibitin 2. Furthermore hnRNP A2/B1 and dynamin 2 interaction with mTORC1 was confirmed on immunoblotting.
NCL disease mechanisms.
Christchurch, New Zealand. In Biochim Biophys Acta, Nov 2013
Despite the identification of a large number of disease-causing genes in recent years, it is still unclear what disease mechanisms operate in the neuronal ceroid lipofuscinoses (NCLs, Batten disease).
RSV fusion: time for a new model.
Toronto, Canada. In Viruses, Mar 2013
In this review we propose a partially hypothetical model of respiratory syncytial virus (RSV) binding and entry to the cell that includes the recently discovered RSV receptor nucleolin, in an attempt to stimulate further inquiry in this research area.
Mechanisms of RNA-induced toxicity in CAG repeat disorders.
Bonn, Germany. In Cell Death Dis, 2012
These include the sequestration of MBNL1, leading to misregulated splicing; sequestration of nucleolin, leading to reduced cellular rRNA; and sequestration of proteins of the siRNA machinery, resulting in the production of short silencing RNAs that affect gene expression.
NCL Disorders: Frequent Causes of Childhood Dementia.
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In Iran J Child Neurol, 2012
UNLABELLED: Dementia in children or young adults is most frequently caused by neuronal ceroidlipofuscinoses (NCL), a group of incurable lysosomal storage disorders linked by the accumulation of a characteristic intracellular storage material and progressive clinical deterioration, usually in combination with visual loss, epilepsy, and motor decline.
Insulin-like growth factor-I inhibits transcriptional responses of transforming growth factor-beta by phosphatidylinositol 3-kinase/Akt-dependent suppression of the activation of Smad3 but not Smad2.
In PLoS ONE, 2002
... P-PKC-zeta (Abcam, ab76129), Syntaxin 4 (Abcam, ab57841), Vamp2 (Abcam, ab3347), Vimentin (Santacruz, sc73259, Actin (Santacruz, sc-1615), Nucleolin (Santacruz, sc13057), Lamin A (Santacruz, sc-20680), MEF2C (Abcam, ab65252), HDAC4 (Cell Signaling, ...