Jonathan Backer's research while affiliated with Albert Einstein College of Medicine and other places

Publications (10)

Preprint
Full-text available
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monit...
Article
Full-text available
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monit...
Preprint
Full-text available
the PDF can be download freely on pubmed. https://pubmed.ncbi.nlm.nih.gov/33634751/
Cover Page
Full-text available
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monit...
Article
Full-text available
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monit...
Article
Full-text available
Phosphoinositide 3-kinases (PI 3-kinases) are regulated by a diverse range of upstream activators, including receptor tyrosine kinases (RTKs), G-protein-coupled receptors (GPCRs), and small GTPases from the Ras, Rho and Rab families. For the Class IA PI 3-kinase PI3Kβ, two mechanisms for GPCR-mediated regulation have been described: direct binding...
Article
Class I phosphoinositide 3-kinases (PI3Ks) catalyze production of the lipid messenger phosphatidylinositol 3,4,5-trisphosphate (PIP3), which plays a central role in a complex signaling network regulating cell growth, survival, and movement. This network is overactivated in cancer and inflammation, and there is interest in determining the PI3K catal...
Article
The Class III phosphoinositide 3-kinase Vps34 (vacuolar protein sorting 34) plays important roles in endocytic trafficking, macroautophagy, phagocytosis, cytokinesis and nutrient sensing. Recent studies have provided exciting new insights into the structure and regulation of this lipid kinase, and new cellular functions for Vps34 have emerged. This...
Article
Full-text available
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring au...
Article
Full-text available
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monit...

Citations

... This is a convenient method, which is based on the pH sensitivity difference between autolysosomes and autophagosomes and the pH sensitivity differences exhibited by green fluorescent protein (GFP) and red fluorescent protein (mRFP), to monitor progression from autophagosome to autolysosome. 43 The green fluorescence quenches when autophagosome fuses with a lysosome to form autolysosomes, at which time only red fluorescence is detected. Therefore, the colocalization of GFP and mRFP is indicative of autophagosomes, exhibiting yellow in the merged image. ...
... As mentioned above, autophagy is a cellular process aimed at maintaining homeostasis that can remove damaged organelles and dysfunctional compounds (Tan et al. 2016). During autophagy, cells redigest their organelles and proteins, thus helping to maintain the synthesis of macromolecules. ...
... Beclin-1 and LC3-II are essential molecules that signal the onset of autophagy, and many researchers use them to monitor autophagy initiation. Since p62 is an autophagy receptor that links ubiquitinated proteins to LC3 and accumulates in cells when autophagy is inhibited, it serves as an index of autophagic degradation [43]. Although LC3-II and LC3-II/I levels decreased after UNC5B overexpression in vivo, the steady expression of Beclin-1 and simultaneous decrease in p62 indicate that autophagic activation is likely unaffected despite changes in autophagic flux. ...
... The mean mitochondrial length was determined by measuring at least 10-20 individual mitochondria from cells obtained by fluorescence microscopy using Leica LAS AF software. The colocalization analyses of mitochondria and autophagosomes provide an indication of the initiation of mitophagy [26,27]. To quantify early mitophagy, cells were transiently transfected with GFP-LC3 (Beyotime Biotech) and stained with 50 nM MitoTracker Red CMXRos after transfection at least 48 h [28,29]. ...
... Studies in neutrophils and in vitro biochemistry suggest that PI3Kβ is synergistically activated through coincidence detection of RTKs and GβGγ (Houslay et al. 2016;Hashem A. Dbouk et al. 2012). Similarly, Rac1(GTP) and GβGγ have been reported to synergistically activate PI3Kβ in cells (Erami et al. 2017). An enhanced membrane recruitment mechanism is the most prominent model used to explain synergistic activation of PI3Ks. ...
... The selective inhibitors of calcineurin/NFAT pathway CsA (39) and proteasome/NF-kB MG-132/SN-50 (30) showed no effect in response to a-IgE ( Figure 3E). PI3K, p38, and ERK1/2 MAPKs are required for ROS production by neutrophils through NOX2 (40). This led us to test the involvement of these pathways on NOX2 activation. ...
... In this context, the lysosomal and mitochondrial actions need to be harmonized to ensure a successful outcome. Class III PI3K [composed of a Vps34 catalytic subunit and a Vps15 regulatory subunit (Baskaran et al., 2014)] is a crucial player in the coordination of the different steps that define autophagy (Backer, 2016). However, until recently the impact of class III PI3K on mitochondrial function needed further explanation. ...
... Autophagy has emerged as a crucial mechanism of tumor cell death triggered by numerous anticancer drugs [40,41]. TEM is considered the definitive method for assessing autophagy in cells through direct visualization of autophagosome formation, making it the gold standard in research [42,43]. S18 and 5-8F cells exhibited typical characteristics of autophagy with autophagosomes and autolysosomes after treated with BBR for 24 h ( Fig. 2A, B). ...