Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27267497
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Elife
2016 ; 5
(?): ? Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Notch1 regulated autophagy controls survival and suppressor activity of activated
murine T-regulatory cells
#MMPMID27267497
Marcel N
; Sarin A
Elife
2016[Jun]; 5
(?): ? PMID27267497
show ga
Cell survival is one of several processes regulated by the Notch pathway in
mammalian cells. Here we report functional outcomes of non-nuclear Notch
signaling to activate autophagy, a conserved cellular response to nutrient
stress, regulating survival in murine natural T-regulatory cells (Tregs), an
immune subset controlling tolerance and inflammation. Induction of autophagy
required ligand-dependent, Notch intracellular domain (NIC) activity, which
controlled mitochondrial organization and survival of activated Tregs.
Consistently, NIC immune-precipitated Beclin and Atg14, constituents of the
autophagy initiation complex. Further, ectopic expression of an effector of
autophagy (Atg3) or recombinant NIC tagged to a nuclear export signal (NIC-NES),
restored autophagy and suppressor function in Notch1(-/-) Tregs. Furthermore,
Notch1 deficiency in the Treg lineage resulted in immune hyperactivity,
implicating Notch activity in Treg homeostasis. Notch1 integration with
autophagy, revealed in these experiments, holds implications for Notch regulated
cell-fate decisions governing differentiation.
free
free
free
