scholarly journals Forms, Crosstalks, and the Role of Phospholipid Biosynthesis in Autophagy

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Leanne Pereira ◽  
John Paul Girardi ◽  
Marica Bakovic
Keyword(s):  
Phospholipid Synthesis ◽  
Phospholipid Biosynthesis ◽  
Lysosomal Degradation ◽  
Specific Mechanism ◽  
Membrane Formation ◽  
Cytoplasmic Material ◽  
Specific Proteins ◽  
Chaperone Mediated Autophagy ◽  
Periods Of Stress

Autophagy is a highly conserved cellular process occurring during periods of stress to ensure a cell's survival by recycling cytosolic constituents and making products that can be used in energy generation and other essential processes. Three major forms of autophagy exist according to the specific mechanism through which cytoplasmic material is transported to a lysosome. Chaperone-mediated autophagy is a highly selective form of autophagy that delivers specific proteins for lysosomal degradation. Microautophagy is a less selective form of autophagy that occurs through lysosomal membrane invaginations, forming tubes and directly engulfing cytoplasm. Finally, macroautophagy involves formation of new membrane bilayers (autophagosomes) that engulf cytosolic material and deliver it to lysosomes. This review provides new insights on the crosstalks between different forms of autophagy and the significance of bilayer-forming phospholipid synthesis in autophagosomal membrane formation.

scholarly journals Inhibitors of lysosomal function or serum starvation in control or LAMP2 deficient cells do not modify the cellular levels of Parkinson disease-associated DJ-1/PARK 7 protein

2018 ◽  
Author(s):  
Raúl Sánchez-Lanzas ◽  
José G. Castaño
Keyword(s):  
Gene Expression ◽  
Parkinson Disease ◽  
Autosomal Recessive ◽  
Serum Starvation ◽  
Lysosomal Degradation ◽  
Lysosomal Function ◽  
Protein Levels ◽  
Chaperone Mediated Autophagy ◽  
Lamp2 Gene

AbstractMutations in PARK7/DJ-1 gene are associated with familial autosomal recessive Parkinson disease. Recently, lysosomes and chaperone mediated autophagy (CMA) has been reported to participate in the degradation of DJ-1/PARK7 protein. Lamp-2A isoform is considered as the lysosomal receptor for the uptake of proteins being degraded by the CMA pathway. We have used several cell lines with disrupted LAMP2 gene expression and their respective control cells to test the possible role of lysosomal degradation and in particular CMA in DJ-1 /PARK7 degradation. Interruption of LAMP-2 expression did not result in an increase of the steady-state protein levels of DJ-1 /PARK7, as it would have been expected. Furthermore, no change in DJ-1 /PARK7 protein levels were observed upon inhibition of lysosomal function with NH4Cl or NH4Cl plus leupeptin, or after activation of CMA by serum starvation for 24h. Accordingly, we have not found any evidence that DJ-1 /PARK7 protein levels are regulated via lysosomal degradation or the CMA pathway.

scholarly journals The Multifaceted Role of CMA in Glioma: Enemy or Ally?

2021 ◽  
Vol 22 (4) ◽  
pp. 2217
Author(s):  
Alessia Lo Dico ◽  
Cristina Martelli ◽  
Cecilia Diceglie ◽  
Luisa Ottobrini
Keyword(s):  
Protein Unfolding ◽  
Target Protein ◽  
Accessory Proteins ◽  
Catabolic Pathway ◽  
Cell Homeostasis ◽  
Essential Proteins ◽  
The Third ◽  
Specific Proteins ◽  
Chaperone Mediated Autophagy

Chaperone-mediated autophagy (CMA) is a catabolic pathway fundamental for cell homeostasis, by which specific damaged or non-essential proteins are degraded. CMA activity has three main levels of regulation. The first regulatory level is based on the targetability of specific proteins possessing a KFERQ-like domain, which can be recognized by specific chaperones and delivered to the lysosomes. Target protein unfolding and translocation into the lysosomal lumen constitutes the second level of CMA regulation and is based on the modulation of Lamp2A multimerization. Finally, the activity of some accessory proteins represents the third regulatory level of CMA activity. CMA’s role in oncology has not been fully clarified covering both pro-survival and pro-death roles in different contexts. Taking all this into account, it is possible to comprehend the actual complexity of both CMA regulation and the cellular consequences of its activity allowing it to be elected as a modulatory and not only catabolic machinery. In this review, the role covered by CMA in oncology is discussed with a focus on its relevance in glioma. Molecular correlates of CMA importance in glioma responsiveness to treatment are described to identify new early efficacy biomarkers and new therapeutic targets to overcome resistance.

scholarly journals The Impact of Autophagy on The Differentiation of Immune Cells

2021 ◽  
Vol 6 (2) ◽  
Keyword(s):  
Immune Cells ◽  
Immune Cell ◽  
Degradation Pathway ◽  
Lysosomal Degradation ◽  
Specific Mechanism ◽  
Multiple Functions ◽  
Selective Degradation ◽  
Proliferation And Differentiation ◽  
The Impact

Autophagy, as a conservative lysosomal degradation pathway, has been well studied for its multiple functions in the immune system. Autophagy has been gradually explored for the regulation of immune cell differentiation. In order to explore the specific mechanism, it is necessary to summarize the role of autophagy in the proliferation and differentiation of immune cells. It is summarized the effects of autophagy in some researches on the function and differentiation of immune cells by introducing the function of autophagy selective degradation. In this review, we discuss the effect of autophagy in the differentiation of immune cells.

scholarly journals Differences in Salivary Proteins as a Function of PROP Taster Status and Gender in Normal Weight and Obese Subjects

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2244
Author(s):  
Melania Melis ◽  
Mariano Mastinu ◽  
Stefano Pintus ◽  
Tiziana Cabras ◽  
Roberto Crnjar ◽  
...  
Keyword(s):  
Food Preferences ◽  
Specific Weight ◽  
Normal Weight ◽  
Nutrition Status ◽  
Salivary Proteins ◽  
Specific Proteins ◽  
Obese Subjects ◽  
And Gender ◽  
Cystatin Sn

Taste plays an important role in processes such as food choices, nutrition status and health. Salivary proteins contribute to taste sensitivity. Taste reduction has been associated with obesity. Gender influences the obesity predisposition and the genetic ability to perceive the bitterness of 6-n-propylthiouracil (PROP), oral marker for food preferences and consumption. We investigated variations in the profile of salivary proteome, analyzed by HPLC-ESI-MS, between sixty-one normal weight subjects (NW) and fifty-seven subjects with obesity (OB), based on gender and PROP sensitivity. Results showed variations of taste-related salivary proteins between NW and OB, which were differently associated with gender and PROP sensitivity. High levels of Ps-1, II-2 and IB-1 proteins belonging to basic proline rich proteins (bPRPs) and PRP-1 protein belonging to acid proline rich proteins (aPRPs) were found in OB males, who showed a lower body mass index (BMI) than OB females. High levels of Ps-1 protein and Cystatin SN (Cyst SN) were found in OB non-tasters, who had lower BMI than OB super-tasters. These new insights on the role of salivary proteins as a factor driving the specific weight gain of OB females and super-tasters, suggest the use of specific proteins as a strategic tool modifying taste responses related to eating behavior.

scholarly journals Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Human Herpesviruses Are Back!

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 185
Author(s):  
Maria Eugenia Ariza
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Disease Process ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Barr Virus ◽  
Fatigue Syndrome ◽  
Specific Proteins ◽  
Epstein Barr ◽  
Human Herpesviruses

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) or Systemic Exertion Intolerance Disease (SEID) is a chronic multisystem illness of unconfirmed etiology. There are currently no biomarkers and/or signatures available to assist in the diagnosis of the syndrome and while numerous mechanisms have been hypothesized to explain the pathology of ME/CFS, the triggers and/or drivers remain unknown. Initial studies suggested a potential role of the human herpesviruses especially Epstein-Barr virus (EBV) in the disease process but inconsistent and conflicting data led to the erroneous suggestion that these viruses had no role in the syndrome. New studies using more advanced approaches have now demonstrated that specific proteins encoded by EBV could contribute to the immune and neurological abnormalities exhibited by a subgroup of patients with ME/CFS. Elucidating the role of these herpesvirus proteins in ME/CFS may lead to the identification of specific biomarkers and the development of novel therapeutics.

The role of exploratory mechanisms in evolution

1995 ◽  
Vol 349 (1329) ◽  
pp. 297-297
Keyword(s):  
Dynamic Instability ◽  
Specific Mechanism ◽  
Cellular Mechanisms ◽  
Selection Processes ◽  
Wide Range ◽  
Rapid Changes ◽  
Neuronal Processes ◽  
History Of ◽  
Variation And Selection

Many cellular mechanisms use a process of variation and selection to generate specific patterns. Among these, dynamic instability of microtubules has been shown to employ a specific mechanism to intentionally generate variation. In many systems the growth of neurons or neuronal processes is excessive, the final connections being established by stabilization of functional interactions. When changes in neuronal networks take place, such as in metamorphosis, use is made of the plasticity of neuronal connectivity. In the immune system, specific responses are generated by variation and selection. Processes that explore a wide range of conditions and a wide range of structures can be called exploratory processes. These are very robust and capable of responding to damage, variability in the environment and ontogenic changes in the organisms. Such robustness would be useful for adapting to changes that occur during phylogenetic changes as well. Given the extensive history of extinction and radiation in evolution, it may be supposed that these mechanisms have themselves been selected for their capacity to survive rapid changes in the organism and for their ability to generate cellular variation.

scholarly journals Impairment of chaperone‐mediated autophagy leads to selective lysosomal degradation defects in the lysosomal storage disease cystinosis

2015 ◽  
Vol 7 (2) ◽  
pp. 158-174 ◽  
Author(s):  
Gennaro Napolitano ◽  
Jennifer L Johnson ◽  
Jing He ◽  
Celine J Rocca ◽  
Jlenia Monfregola ◽  
...  
Keyword(s):  
Lysosomal Storage Disease ◽  
Storage Disease ◽  
Lysosomal Storage ◽  
Lysosomal Degradation ◽  
Chaperone Mediated Autophagy

scholarly journals News about the Role of Fluid and Imaging Biomarkers in Neurodegenerative Diseases

Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 252
Author(s):  
Jacopo Meldolesi
Keyword(s):  
Neurodegenerative Diseases ◽  
Imaging Techniques ◽  
Imaging Biomarkers ◽  
Positron Emission ◽  
Specific Proteins ◽  
Great Relevance ◽  
The Brain ◽  
Positive Point

Biomarkers are molecules that are variable in their origin, nature, and mechanism of action; they are of great relevance in biology and also in medicine because of their specific connection with a single or several diseases. Biomarkers are of two types, which in some cases are operative with each other. Fluid biomarkers, started around 2000, are generated in fluid from specific proteins/peptides and miRNAs accumulated within two extracellular fluids, either the central spinal fluid or blood plasma. The switch of these proteins/peptides and miRNAs, from free to segregated within extracellular vesicles, has induced certain advantages including higher levels within fluids and lower operative expenses. Imaging biomarkers, started around 2004, are identified in vivo upon their binding by radiolabeled molecules subsequently revealed in the brain by positron emission tomography and/or other imaging techniques. A positive point for the latter approach is the quantitation of results, but expenses are much higher. At present, both types of biomarker are being extensively employed to study Alzheimer’s and other neurodegenerative diseases, investigated from the presymptomatic to mature stages. In conclusion, biomarkers have revolutionized scientific and medical research and practice. Diagnosis, which is often inadequate when based on medical criteria only, has been recently improved by the multiplicity and specificity of biomarkers. Analogous results have been obtained for prognosis. In contrast, improvement of therapy has been limited or fully absent, especially for Alzheimer’s in which progress has been inadequate. An urgent need at hand is therefore the progress of a new drug trial design together with patient management in clinical practice.

scholarly journals The Role of Chaperone-Mediated Autophagy in Hepatitis C Virus-Induced Pathogenesis

2021 ◽  
Vol 11 ◽  
Author(s):  
Chieko Matsui ◽  
Putu Yuliandari ◽  
Lin Deng ◽  
Takayuki Abe ◽  
Ikuo Shoji
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Degradation Process ◽  
Degradation Pathway ◽  
Hepatocyte Nuclear Factor ◽  
Selective Degradation ◽  
Substrate Protein ◽  
Hepatocyte Nuclear Factor 1Α ◽  
Chaperone Mediated Autophagy

Lysosome incorporate and degrade proteins in a process known as autophagy. There are three types of autophagy; macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Although autophagy is considered a nonselective degradation process, CMA is known as a selective degradation pathway. All proteins internalized in the lysosome via CMA contain a pentapeptide KFERQ-motif, also known as a CMA-targeting motif, which is necessary for selectivity. CMA directly delivers a substrate protein into the lysosome lumen using the cytosolic chaperone HSC70 and the lysosomal receptor LAMP-2A for degradation. Hepatitis C virus (HCV) NS5A protein interacts with hepatocyte-nuclear factor 1α (HNF-1α) together with HSC70 and promotes the lysosomal degradation of HNF-1α via CMA, resulting in HCV-induced pathogenesis. HCV NS5A promotes recruitment of HSC70 to the substrate protein HNF-1α. HCV NS5A plays a crucial role in HCV-induced CMA. Further investigations of HCV NS5A-interacting proteins containing CMA-targeting motifs may help to elucidate HCV-induced pathogenesis.

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