Microreviews
GFI1’s role in DNA repair suggests implications for tumour cell response to treatment
Charles Vadnais1 and Tarik Möröy1,2,3
GFI1 was discovered over 20 years ago and a large body of experimental evidence defines its function as a DNA binding transcriptional repressor. Since GFI1 does not possess any enzymatic
Amelioration of obesity-induced diabetes by a novel autophagy enhancer
Hyejin Lim1 and Myung-Shik Lee1
Our screening system was a convenient high throughput assay of autophagic flux rather than cumulative autophagy levels, and the index of autophagic activity was calculated as the ratio of the
Striatal dual cholinergic /GABAergic transmission in Parkinson disease: friends or foes?
Natalia Lozovaya1, Yehezkel Ben-Ari1 and Constance Hammond1
Although constituting less than 1% of neuronal population of the striatum, cholinergic interneurons play a major role in the control of sensory integration in preparation for movements. These giant neurons
The NLRC4 inflammasome requires IRF8-dependent production of NAIPs
Ein Lee1,2, Rajendra Karki1 and Thirumala-Devi Kanneganti1
Inflammasomes orchestrate cellular responses to pathogen- or danger-associated molecular patterns by controlling the activation of caspase-1. Inflammasome activation results in enzymatically active caspase-1, which mediates the maturation and release of
Targeting LRH-1/NR5A2 to treat type 1 diabetes mellitus
Nadia Cobo-Vuilleumier1, Petra I. Lorenzo1 and Benoit R. Gauthier1
The liver receptor homolog-1 (LRH-1) is a member of the NR5A family of nuclear receptors that plays a pivotal role in early embryonic development while later on it specifies the
Calling RNF168 to action
Somaira Nowsheen1 and Zhenkun Lou2
– [table id=103 /] – It is interesting to note that MDC1 acts as a node for the recruitment of both RNF8 and L3MBTL2 and brings these two factors into
Exosomal secretion of truncated cytosolic lysyl-tRNA synthetase induces inflammation during cell starvation
Sang Bum Kim1,2, Seongmin Cho1, 2 and Sunghoon Kim1,2
Kim et al. (2017) reveals three crucial steps of KRS secretion, including its dissociation from the MSC complex, interaction with syntenin, and secretion via the exosomal pathway (Figure 1). –
Endolysosomal dysfunction and exosome secretion: implications for neurodegenerative disorders
André M. Miranda1,2,3,4 and Gilbert Di Paolo1,2,5
A master regulator of both endolysosomal function and autophagy is Vps34 and its lipid product phosphatidylinositol-3-phosphate (PI3P) through which the lipid kinase exerts most of its biological actions in eukaryotic
Oxidation of p62 as an evolutionary adaptation to promote autophagy in stress conditions
Elsje G. Otten1,§, Rhoda Stefanatos1, Bernadette Carroll1, Viktor I. Korolchuk1
Autophagy (literally meaning self-eating) is an intracellular trafficking pathway. It involves the formation of a double membraned organelle (called the autophagosome) around components of the cell, such as damaged proteins,