Maxwellpeck7489

ere is a significant enrichment in SP cells among different EC cell lines, and these SP cells be more resistant to Taxol, MPA and radiation therapy. The overexpression of BCRP among SP cells may be the cause of resistance to Taxol, progestin and radiotherapy, which may be related to apoptosis and autophagic activity. Copyright © 2020 Liu, Xu, Yu, Li, Yao, Zhao, Wang, Wei and Li.Mitophagy, a conserved intracellular process by which mitochondria are eliminated via the autophagic machinery, is a quality control mechanism which facilitates maintenance of a functional mitochondrial network and cell homeostasis, making it a key process in development and longevity. Mitophagy has been linked to multiple human disorders, especially neurodegenerative diseases where the long-lived neurons are relying on clearance of old/damaged mitochondria to survive. During the past decade, the availability of novel tools to study mitophagy both in vitro and in vivo has significantly advanced our understanding of the molecular mechanisms governing this fundamental process in normal physiology and in various disease models. We here give an overview of the known mitophagy pathways and how they are induced, with a particular emphasis on the early events governing mitophagosome formation. Copyright © 2020 Zachari and Ktistakis.Developmental gene regulatory networks (GRNs) underpin metazoan embryogenesis and have undergone substantial modification to generate the tremendous variety of animal forms present on Earth today. The nematode Caenorhabditis elegans has been a central model for advancing many important discoveries in fundamental mechanistic biology and, more recently, has provided a strong base from which to explore the evolutionary diversification of GRN architecture and developmental processes in other species. In this short review, we will focus on evolutionary diversification of the GRN for the most ancient of the embryonic germ layers, the endoderm. Early embryogenesis diverges considerably across the phylum Nematoda. Notably, while some species deploy regulative development, more derived species, such as C. elegans, exhibit largely mosaic modes of embryogenesis. Despite the relatively similar morphology of the nematode gut across species, widespread variation has been observed in the signaling inputs that initiate the endoderm GRN, an exemplar of developmental system drift (DSD). We will explore how genetic variation in the endoderm GRN helps to drive DSD at both inter- and intraspecies levels, thereby resulting in a robust developmental system. Comparative studies using divergent nematodes promise to unveil the genetic mechanisms controlling developmental plasticity and provide a paradigm for the principles governing evolutionary modification of an embryonic GRN. Copyright © 2020 Ewe, Torres Cleuren and Rothman.Homotypic and heterotypic interactions between cells are of crucial importance in multicellular organisms for the maintenance of physiological functions. Accordingly, changes in cell-to-cell communication contribute significantly to tumor development. Cancer cells engage the different components of the tumor microenvironment (TME) to support malignant proliferation, escape immune control, and favor metastatic spreading. The interaction between cancerous and non-cancerous cell types within tumors occurs in many ways, including physical contact and paracrine signaling. Furthermore, local and long-range transfer of biologically active molecules (e.g., DNA, RNA, and proteins) can be mediated by small extracellular vesicles (EVs) and this has been shown to influence many aspects of tumor progression. As it stands, there is a critical need for suitable experimental systems that enable modeling the cell-to-cell communications occurring in cancer. Given their intrinsic complexity, animal models represent the ideal syhe potential of using organoids to model the interplay between cancer and non-cancer cells in order to unveil biological mechanisms involved in cancers initiation and progression, which might ultimately lead to the identification of novel intervention strategy for those diseases. Copyright © 2020 Fiorini, Veghini and Corbo.Retrograde transport from endosomes to the trans-Golgi network (TGN) diverts proteins and lipids away from lysosomal degradation. It is essential for maintaining cellular homeostasis and signaling. In recent years, significant advancements have been made in understanding this classical pathway, revealing new insights into multiple steps of vesicular trafficking as well as critical roles of ER-endosome contacts for endosomal trafficking. In this review, we summarize up-to-date knowledge about this trafficking pathway, in particular, mechanisms of cargo recognition at endosomes and vesicle tethering at the TGN, and contributions of ER-endosome contacts. Copyright © 2020 Tu, Zhao, Billadeau and Jia.The immune checkpoint blockade therapy has drastically advanced treatment of different types of cancer over the past few years. Female breast cancer is the second leading cause of death in the overall burden of cancers worldwide that is encouraging healthcare professionals to improve cancer care management. SKF96365 The checkpoint blockade therapies combined with novel agents become the recent focus of various clinical trials in breast cancer. However, identification of the patients who are responsive to these therapeutic strategies remained as a major issue for enhancing the efficacy of these treatments. This highlights the unmet need in discovery and development of novel biomarkers to add predictive values for prosperous personalized medicine. In this review we summarize the advances done in the era of biomarker studies and highlight their link in supporting breast cancer immunotherapy. Copyright © 2020 Vafaizadeh and Barekati.Historically synemin has been studied as an intermediate filament protein. However, synemin also binds the type II regulatory (R) subunit α of protein kinase A (PKA) and protein phosphatase type 2A, thus participating in the PKA and phosphoinositide 3-kinase (PI3K)-Akt and signaling pathways. In addition, recent studies using transgenic mice indicate that a significant function of synemin is its role in signaling pathways in various tissues, including the heart. Recent clinical reports have shown that synemin mutations led to multiple cases of dilated cardiomyopathy. Additionally, a single case of the rare condition ulnar-mammary-like syndrome with left ventricular tachycardia due to a mutation in the synemin gene (SYNM) has been reported. Therefore, this review uses these recent studies to provide a new framework for detailed discussions on synemin tissue distribution, binding partners and synemin in disease. Differences between α- and β-synemin are highlighted. The studies presented here indicate that while synemin does function as an intermediate filament protein, it is unique among this large family of proteins as it is also a regulator of signaling pathways and a crosslinker.