Log in

Relevant bibliographies by topics / Autophagic receptors / Journal articles

To see the other types of publications on this topic, follow the link: Autophagic receptors.

Journal articles on the topic 'Autophagic receptors'

Author: Grafiati

Published: 13 April 2024

Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Autophagic receptors.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Pino-Belmar, Camila, Rayén Aguilar, Guillermo E. Valenzuela-Nieto, et al. "An Intrinsic Host Defense against HSV-1 Relies on the Activation of Xenophagy with the Active Clearance of Autophagic Receptors." Cells 13, no. 15 (2024): 1256. http://dx.doi.org/10.3390/cells13151256.

Full text

Abstract:

Autophagy engulfs cellular components in double-membrane-bound autophagosomes for clearance and recycling after fusion with lysosomes. Thus, autophagy is a key process for maintaining proteostasis and a powerful cell-intrinsic host defense mechanism, protecting cells against pathogens by targeting them through a specific form of selective autophagy known as xenophagy. In this context, ubiquitination acts as a signal of recognition of the cargoes for autophagic receptors, which direct them towards autophagosomes for subsequent breakdown. Nevertheless, autophagy can carry out a dual role since n

APA, Harvard, Vancouver, ISO, and other styles

2

Kimura, Tomonori, Ashish Jain, Seong Won Choi, et al. "TRIM-mediated precision autophagy targets cytoplasmic regulators of innate immunity." Journal of Cell Biology 210, no. 6 (2015): 973–89. http://dx.doi.org/10.1083/jcb.201503023.

Full text

Abstract:

The present paradigms of selective autophagy in mammalian cells cannot fully explain the specificity and selectivity of autophagic degradation. In this paper, we report that a subset of tripartite motif (TRIM) proteins act as specialized receptors for highly specific autophagy (precision autophagy) of key components of the inflammasome and type I interferon response systems. TRIM20 targets the inflammasome components, including NLRP3, NLRP1, and pro–caspase 1, for autophagic degradation, whereas TRIM21 targets IRF3. TRIM20 and TRIM21 directly bind their respective cargo and recruit autophagic

APA, Harvard, Vancouver, ISO, and other styles

3

Kim, Eun Young, and Jae Man Lee. "Liver Metabolism at the Crossroads: The Reciprocal Control of Nutrient-Sensing Nuclear Receptors and Autophagy." International Journal of Molecular Sciences 26, no. 12 (2025): 5825. https://doi.org/10.3390/ijms26125825.

Full text

Abstract:

Peroxisome proliferator-activated receptor α (PPARα, encoded by NR1C1) and farnesoid X receptor (FXR, encoded by NR1H4) are the two prominent nutrient-sensing nuclear receptors essential for maintaining hepatic metabolism during fasting and fed states, respectively. These nuclear receptors comprehensively regulate the transcription of numerous genes involved in fatty acid oxidation (FAO), ketogenesis, bile acid (BA) biosynthesis, and other metabolic processes critical for liver energy homeostasis. These receptors have been shown to have opposite impacts on autophagy, which is triggered by PPAR

APA, Harvard, Vancouver, ISO, and other styles

4

Lin, Long, Peiguo Yang, Xinxin Huang, Hui Zhang, Qun Lu, and Hong Zhang. "The scaffold protein EPG-7 links cargo–receptor complexes with the autophagic assembly machinery." Journal of Cell Biology 201, no. 1 (2013): 113–29. http://dx.doi.org/10.1083/jcb.201209098.

Full text

Abstract:

The mechanism by which protein aggregates are selectively degraded by autophagy is poorly understood. Previous studies show that a family of Atg8-interacting proteins function as receptors linking specific cargoes to the autophagic machinery. Here we demonstrate that during Caenorhabditis elegans embryogenesis, epg-7 functions as a scaffold protein mediating autophagic degradation of several protein aggregates, including aggregates of the p62 homologue SQST-1, but has little effect on other autophagy-regulated processes. EPG-7 self-oligomerizes and is degraded by autophagy independently of SQS

APA, Harvard, Vancouver, ISO, and other styles

5

Luo, Shuwei, Xifeng Li, Yan Zhang, et al. "Cargo Recognition and Function of Selective Autophagy Receptors in Plants." International Journal of Molecular Sciences 22, no. 3 (2021): 1013. http://dx.doi.org/10.3390/ijms22031013.

Full text

Abstract:

Autophagy is a major quality control system for degradation of unwanted or damaged cytoplasmic components to promote cellular homeostasis. Although non-selective bulk degradation of cytoplasm by autophagy plays a role during cellular response to nutrient deprivation, the broad roles of autophagy are primarily mediated by selective clearance of specifically targeted components. Selective autophagy relies on cargo receptors that recognize targeted components and recruit them to autophagosomes through interaction with lapidated autophagy-related protein 8 (ATG8) family proteins anchored in the me

APA, Harvard, Vancouver, ISO, and other styles

6

Chang, Chunmei, Xiaoshan Shi, Liv E. Jensen, et al. "Reconstitution of cargo-induced LC3 lipidation in mammalian selective autophagy." Science Advances 7, no. 17 (2021): eabg4922. http://dx.doi.org/10.1126/sciadv.abg4922.

Full text

Abstract:

Selective autophagy of damaged mitochondria, protein aggregates, and other cargoes is essential for health. Cargo initiates phagophore biogenesis, which entails the conjugation of LC3 to phosphatidylethanolamine. Current models suggest that clustered ubiquitin chains on a cargo trigger a cascade from autophagic cargo receptors through the core complexes ULK1 and class III phosphatidylinositol 3-kinase complex I, WIPI2, and the ATG7, ATG3, and ATG12ATG5-ATG16L1 machinery of LC3 lipidation. This was tested using giant unilamellar vesicles (GUVs), GST-Ub4 as a model cargo, the cargo receptors NDP

APA, Harvard, Vancouver, ISO, and other styles

7

Valenzuela, Cristián A., Marco Azúa, Claudio A. Álvarez, Paulina Schmitt, Nicolás Ojeda, and Luis Mercado. "Evidence of the Autophagic Process during the Fish Immune Response of Skeletal Muscle Cells against Piscirickettsia salmonis." Animals 13, no. 5 (2023): 880. http://dx.doi.org/10.3390/ani13050880.

Full text

Abstract:

Autophagy is a fundamental cellular process implicated in the health of the cell, acting as a cytoplasmatic quality control machinery by self-eating unfunctional organelles and protein aggregates. In mammals, autophagy can participate in the clearance of intracellular pathogens from the cell, and the activity of the toll-like receptors mediates its activation. However, in fish, the modulation of autophagy by these receptors in the muscle is unknown. This study describes and characterizes autophagic modulation during the immune response of fish muscle cells after a challenge with intracellular

APA, Harvard, Vancouver, ISO, and other styles

8

Papandreou, Margarita-Elena, and Nektarios Tavernarakis. "Selective Autophagy as a Potential Therapeutic Target in Age-Associated Pathologies." Metabolites 11, no. 9 (2021): 588. http://dx.doi.org/10.3390/metabo11090588.

Full text

Abstract:

Progressive accumulation of damaged cellular constituents contributes to age-related diseases. Autophagy is the main catabolic process, which recycles cellular material in a multitude of tissues and organs. Autophagy is activated upon nutrient deprivation, and oncogenic, heat or oxidative stress-induced stimuli to selectively degrade cell constituents and compartments. Specificity and accuracy of the autophagic process is maintained via the precision of interaction of autophagy receptors or adaptors and substrates by the intricate, stepwise orchestration of specialized integrating stimuli. Pol

APA, Harvard, Vancouver, ISO, and other styles

9

Skendros, Panagiotis, and Ioannis Mitroulis. "Host Cell Autophagy in Immune Response to Zoonotic Infections." Clinical and Developmental Immunology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/910525.

Full text

Abstract:

Autophagy is a fundamental homeostatic process in which cytoplasmic targets are sequestered within double-membraned autophagosomes and subsequently delivered to lysosomes for degradation. Accumulating evidence supports the pivotal role of autophagy in host defense against intracellular pathogens implicating both innate and adaptive immunity. Many of these pathogens cause common zoonotic infections worldwide. The induction of the autophagic machinery by innate immune receptors signaling, such as TLRs, NOD1/2, and p62/SQSTM1 in antigen-presenting cells results in inhibition of survival and elimi

APA, Harvard, Vancouver, ISO, and other styles

10

Li, Hongli, Celien Lismont, Cláudio F. Costa, Mohamed A. F. Hussein, Myriam Baes, and Marc Fransen. "Enhanced Levels of Peroxisome-Derived H2O2 Do Not Induce Pexophagy but Impair Autophagic Flux in HEK-293 and HeLa Cells." Antioxidants 12, no. 3 (2023): 613. http://dx.doi.org/10.3390/antiox12030613.

Full text

Abstract:

Peroxisomes are functionally specialized organelles that harbor multiple hydrogen peroxide (H2O2)-producing and -degrading enzymes. Given that this oxidant functions as a major redox signaling agent, peroxisomes have the intrinsic ability to mediate and modulate H2O2-driven processes, including autophagy. However, it remains unclear whether changes in peroxisomal H2O2 (po-H2O2) emission impact the autophagic process and to which extent peroxisomes with a disturbed H2O2 metabolism are selectively eliminated through a process called “pexophagy”. To address these issues, we generated and validate

APA, Harvard, Vancouver, ISO, and other styles

11

Wang, Wang-sheng, Wen-jiao Li, Ya-wei Wang, et al. "Involvement of serum amyloid A1 in the rupture of fetal membranes through induction of collagen I degradation." Clinical Science 133, no. 3 (2019): 515–30. http://dx.doi.org/10.1042/cs20180950.

Full text

Abstract:

Abstract The de novo synthesis of serum amyloid A1 (SAA1) is augmented in human fetal membranes at parturition. However, its role in parturition remains largely unknown. Here, we investigated whether SAA1 was involved in the rupture of fetal membranes, a crucial event in parturition accompanied with extensive degradation of collagens. Results showed that SAA1 decreased both intracellular and extracellular COL1A1 and COL1A2 abundance, the two subunits of collagen I, without affecting their mRNA levels in human amnion fibroblasts. These reductions were completely blocked only with inhibition of

APA, Harvard, Vancouver, ISO, and other styles

12

Cheng, Li-sha, Jing Li, Yun Liu, et al. "HMGB1-induced autophagy: a new pathway to maintain Treg function during chronic hepatitis B virus infection." Clinical Science 131, no. 5 (2017): 381–94. http://dx.doi.org/10.1042/cs20160704.

Full text

Abstract:

High-mobility group box-1 (HMGB1) protein, as one of the well-known damage-associated molecular pattern molecules (DAMPs), is enriched in chronic hepatitis B virus (HBV) infection and has a context-dependent role in autophagy, a highly conserved self-digestive process in response to environmental stress. Recent mouse studies indicate that autophagy is highly active in regulatory T (Treg)-cells. In the present study, we evaluated spontaneous and induced autophagy of peripheral Treg cells from 98 patients with chronic hepatitis B (CHB), by measuring levels of lipidated form of microtubule-associ

APA, Harvard, Vancouver, ISO, and other styles

13

Takahashi, Shun-saku, Yu-Shin Sou, Tetsuya Saito, et al. "Loss of autophagy impairs physiological steatosis by accumulation of NCoR1." Life Science Alliance 3, no. 1 (2019): e201900513. http://dx.doi.org/10.26508/lsa.201900513.

Full text

Abstract:

Lipid droplets (LDs) are dynamic organelles that store neutral lipids during times of energy excess, such as after a meal. LDs serve as an energy reservoir during fasting and have a buffering capacity that prevents lipotoxicity. Autophagy and the autophagic machinery have been proposed to play a role in LD biogenesis, but the underlying molecular mechanism remains unclear. Here, we show that when nuclear receptor co-repressor 1 (NCoR1), which inhibits the transactivation of nuclear receptors, accumulates because of autophagy suppression, LDs decrease in size and number. Ablation of ATG7, a gen

APA, Harvard, Vancouver, ISO, and other styles

14

LING, PIN, Kuan-Ru Chen, Chen-Chu Kao, Huai-Chia Chuang, and Tse-Hua Tan. "Emerging roles of an innate immune regulator TAPE in Toll-like receptors, RIG-I-like receptors, and beyond." Journal of Immunology 196, no. 1_Supplement (2016): 202.35. http://dx.doi.org/10.4049/jimmunol.196.supp.202.35.

Full text

Abstract:

Abstract Pattern-recognition receptors (PRRs) trigger innate immune defenses against pathogen infection via downstream signaling pathways linking to inflammation and cell-autonomous immunity like phagocytosis and autophagy. IKK family kinases, IKKα and IKKβ, function to relay PRR signals to proinflammatory cytokine production to amplify innate immune responses. TBK1, a non-canonical IKK kinase, links nucleic acid sensors to type I interferon induction against viral infection and also regulates the autophagic clearance of intracellular bacteria. TBK1-Associated Protein in Endolysosomes designat

APA, Harvard, Vancouver, ISO, and other styles

15

Rogov, Vladimir V., Hironori Suzuki, Evgenij Fiskin, et al. "Structural basis for phosphorylation-triggered autophagic clearance of Salmonella." Biochemical Journal 454, no. 3 (2013): 459–66. http://dx.doi.org/10.1042/bj20121907.

Full text

Abstract:

Selective autophagy is mediated by the interaction of autophagy modifiers and autophagy receptors that also bind to ubiquitinated cargo. Optineurin is an autophagy receptor that plays a role in the clearance of cytosolic Salmonella. The interaction between receptors and modifiers is often relatively weak, with typical values for the dissociation constant in the low micromolar range. The interaction of optineurin with autophagy modifiers is even weaker, but can be significantly enhanced through phosphorylation by the TBK1 {TANK [TRAF (tumour-necrosis-factor-receptor-associated factor)-associate

APA, Harvard, Vancouver, ISO, and other styles

16

Eskelinen, Eeva-Liisa, Anna Lena Illert, Yoshitaka Tanaka, et al. "Role of LAMP-2 in Lysosome Biogenesis and Autophagy." Molecular Biology of the Cell 13, no. 9 (2002): 3355–68. http://dx.doi.org/10.1091/mbc.e02-02-0114.

Full text

Abstract:

In LAMP-2–deficient mice autophagic vacuoles accumulate in many tissues, including liver, pancreas, muscle, and heart. Here we extend the phenotype analysis using cultured hepatocytes. In LAMP-2–deficient hepatocytes the half-life of both early and late autophagic vacuoles was prolonged as evaluated by quantitative electron microscopy. However, an endocytic tracer reached the autophagic vacuoles, indicating delivery of endo/lysosomal constituents to autophagic vacuoles. Enzyme activity measurements showed that the trafficking of some lysosomal enzymes to lysosomes was impaired. Immunoprecipita

APA, Harvard, Vancouver, ISO, and other styles

17

Kohno, Shohei, Yuji Shiozaki, Audrey L. Keenan, Shinobu Miyazaki-Anzai, and Makoto Miyazaki. "An N-terminal–truncated isoform of FAM134B (FAM134B-2) regulates starvation-induced hepatic selective ER-phagy." Life Science Alliance 2, no. 3 (2019): e201900340. http://dx.doi.org/10.26508/lsa.201900340.

Full text

Abstract:

Autophagy is a conserved system that adapts to nutrient starvation, after which proteins and organelles are degraded to recycle amino acids in response to starvation. Recently, the ER was added to the list of targets of autophagic degradation. Autophagic degradation pathways of bulk ER and the specific proteins sorted through the ER are considered key mechanisms in maintaining ER homeostasis. Four ER-resident proteins (FAM134B, CCPG1, SEC62, and RTN3) have been identified as ER-resident cargo receptors, which contain LC3-interacting regions. In this study, we identified an N-terminal–truncated

APA, Harvard, Vancouver, ISO, and other styles

18

Mejlvang, Jakob, Hallvard Olsvik, Steingrim Svenning, et al. "Starvation induces rapid degradation of selective autophagy receptors by endosomal microautophagy." Journal of Cell Biology 217, no. 10 (2018): 3640–55. http://dx.doi.org/10.1083/jcb.201711002.

Full text

Abstract:

It is not clear to what extent starvation-induced autophagy affects the proteome on a global scale and whether it is selective. In this study, we report based on quantitative proteomics that cells during the first 4 h of acute starvation elicit lysosomal degradation of up to 2–3% of the proteome. The most significant changes are caused by an immediate autophagic response elicited by shortage of amino acids but executed independently of mechanistic target of rapamycin and macroautophagy. Intriguingly, the autophagy receptors p62/SQSTM1, NBR1, TAX1BP1, NDP52, and NCOA4 are among the most efficie

APA, Harvard, Vancouver, ISO, and other styles

19

Shrestha, Birendra Kumar, Mads Skytte Rasmussen, Yakubu Princely Abudu, et al. "NIMA-related kinase 9–mediated phosphorylation of the microtubule-associated LC3B protein at Thr-50 suppresses selective autophagy of p62/sequestosome 1." Journal of Biological Chemistry 295, no. 5 (2019): 1240–60. http://dx.doi.org/10.1074/jbc.ra119.010068.

Full text

Abstract:

Human ATG8 family proteins (ATG8s) are active in all steps of the macroautophagy pathway, and their lipidation is essential for autophagosome formation. Lipidated ATG8s anchored to the outer surface of the phagophore serve as scaffolds for binding of other core autophagy proteins and various effector proteins involved in trafficking or fusion events, whereas those at the inner surface are needed for assembly of selective autophagy substrates. Their scaffolding role depends on specific interactions between the LC3-interacting region (LIR) docking site (LDS) in ATG8s and LIR motifs in various in

APA, Harvard, Vancouver, ISO, and other styles

20

García Porta, Cloe, Kashif Mahfooz, Joanna Komorowska, Sara Garcia-Rates, and Susan Greenfield. "A Novel 14mer Peptide Inhibits Autophagic Flux via Selective Activation of the mTORC1 Signalling Pathway: Implications for Alzheimer’s Disease." International Journal of Molecular Sciences 25, no. 23 (2024): 12837. http://dx.doi.org/10.3390/ijms252312837.

Full text

Abstract:

During development, a 14mer peptide, T14, modulates cell growth via the α-7 nicotinic acetylcholine receptor (α7 nAChR). However, this process could become excitotoxic in the context of the adult brain, leading to pathologies such as Alzheimer’s disease (AD). Recent work shows that T14 acts selectively via the mammalian target of rapamycin complex 1 (mTORC1). This pathway is essential for normal development but is overactive in AD. The triggering of mTORC1 has also been associated with the suppression of autophagy, commonly observed in ageing and neurodegeneration. We therefore investigated th

APA, Harvard, Vancouver, ISO, and other styles

21

Acheampong, Atiako Kwame, Carly Shanks, Chia-Yi Cheng, G. Eric Schaller, Yasin Dagdas, and Joseph J. Kieber. "EXO70D isoforms mediate selective autophagic degradation of type-A ARR proteins to regulate cytokinin sensitivity." Proceedings of the National Academy of Sciences 117, no. 43 (2020): 27034–43. http://dx.doi.org/10.1073/pnas.2013161117.

Full text

Abstract:

The phytohormone cytokinin influences many aspects of plant growth and development, several of which also involve the cellular process of autophagy, including leaf senescence, nutrient remobilization, and developmental transitions. The Arabidopsis type-A response regulators (type-A ARR) are negative regulators of cytokinin signaling that are transcriptionally induced in response to cytokinin. Here, we describe a mechanistic link between cytokinin signaling and autophagy, demonstrating that plants modulate cytokinin sensitivity through autophagic regulation of type-A ARR proteins. Type-A ARR pr

APA, Harvard, Vancouver, ISO, and other styles

22

Morleo, Manuela, and Brunella Franco. "The OFD1 protein is a novel player in selective autophagy: another tile to the cilia/autophagy puzzle." Cell Stress 5, no. 3 (2021): 33–36. http://dx.doi.org/10.15698/cst2021.03.244.

Full text

Abstract:

The autophagy-lysosomal pathway is one of the main degradative routes which cells use to balance sources of energy. A number of proteins orchestrate the formation of autophagosomes, membranous organelles instrumental in autophagy. Selective autophagy, involving the recognition and removal of specific targets, is mediated by autophagy receptors, which recognize cargos and the autophagosomal membrane protein LC3 for lysosomal degradation. Recently, bidirectional crosstalk has emerged between autophagy and primary cilia, microtubule-based sensory organelles extending from cells and anchored by th

APA, Harvard, Vancouver, ISO, and other styles

23

Ran, Jie, Sayed M. Hashimi, and Jian-Zhong Liu. "Emerging Roles of the Selective Autophagy in Plant Immunity and Stress Tolerance." International Journal of Molecular Sciences 21, no. 17 (2020): 6321. http://dx.doi.org/10.3390/ijms21176321.

Full text

Abstract:

Autophagy is a conserved recycling system required for cellular homeostasis. Identifications of diverse selective receptors/adaptors that recruit appropriate autophagic cargoes have revealed critical roles of selective autophagy in different biological processes in plants. In this review, we summarize the emerging roles of selective autophagy in both biotic and abiotic stress tolerance and highlight the new features of selective receptors/adaptors and their interactions with both the cargoes and Autophagy-related gene 8s (ATG8s). In addition, we review how the two major degradation systems, na

APA, Harvard, Vancouver, ISO, and other styles

24

Richter, Benjamin, Danielle A. Sliter, Lina Herhaus, et al. "Phosphorylation of OPTN by TBK1 enhances its binding to Ub chains and promotes selective autophagy of damaged mitochondria." Proceedings of the National Academy of Sciences 113, no. 15 (2016): 4039–44. http://dx.doi.org/10.1073/pnas.1523926113.

Full text

Abstract:

Selective autophagy of damaged mitochondria requires autophagy receptors optineurin (OPTN), NDP52 (CALCOCO2), TAX1BP1, and p62 (SQSTM1) linking ubiquitinated cargo to autophagic membranes. By using quantitative proteomics, we show that Tank-binding kinase 1 (TBK1) phosphorylates all four receptors on several autophagy-relevant sites, including the ubiquitin- and LC3-binding domains of OPTN and p62/SQSTM1 as well as the SKICH domains of NDP52 and TAX1BP1. Constitutive interaction of TBK1 with OPTN and the ability of OPTN to bind to ubiquitin chains are essential for TBK1 recruitment and kinase

APA, Harvard, Vancouver, ISO, and other styles

25

Waters, Sarah L., Katie Marchbank, Ellen Solomon, and Caroline A. Whitehouse. "Autophagic receptors Nbr1 and p62 coregulate skeletal remodelling." Autophagy 6, no. 7 (2010): 981–83. http://dx.doi.org/10.4161/auto.6.7.13155.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Vona, Rosa, Camilla Cittadini, Elena Ortona, and Paola Matarrese. "Sex Disparity in Cancer: Role of Autophagy and Estrogen Receptors." Cells 14, no. 4 (2025): 273. https://doi.org/10.3390/cells14040273.

Full text

Abstract:

Autophagy, a cellular process essential for maintaining homeostasis, plays a fundamental role in recycling damaged components and in adapting to stress. The dysregulation of autophagy is implicated in numerous human diseases, including cancer, where it exhibits a dual role as both a suppressor and a promoter, depending on the context and the stage of tumor development. The significant sex differences observed in autophagic processes are determined by biological factors, such as genetic makeup and sex hormones. Estrogens, through their interaction with specific receptors, modulate autophagy and

APA, Harvard, Vancouver, ISO, and other styles

27

Du, Chunyang, Tao Zhang, Xia Xiao, Yonghong Shi, Huijun Duan, and Yunzhuo Ren. "Protease-activated receptor-2 promotes kidney tubular epithelial inflammation by inhibiting autophagy via the PI3K/Akt/mTOR signalling pathway." Biochemical Journal 474, no. 16 (2017): 2733–47. http://dx.doi.org/10.1042/bcj20170272.

Full text

Abstract:

Protease-activated receptor-2 (PAR2), which belongs to a specific class of the G-protein-coupled receptors, is central to several inflammation processes. However, the precise molecular mechanism involved remains undefined. Autophagy has been previously shown to affect inflammation. In the present study, we examine the effect of PAR2 on kidney tubular epithelial autophagy and on autophagy-related inflammation and reveal the underlying mechanism involved. Autophagic activity and levels of autophagic marker LC3 were examined in human kidney tubular epithelial cells with PAR2 knockdown or overexpr

APA, Harvard, Vancouver, ISO, and other styles

28

Kim, Yi Sak, Prashanta Silwal, Soo Yeon Kim, Tamotsu Yoshimori, and Eun-Kyeong Jo. "Autophagy-activating strategies to promote innate defense against mycobacteria." Experimental & Molecular Medicine 51, no. 12 (2019): 1–10. http://dx.doi.org/10.1038/s12276-019-0290-7.

Full text

Abstract:

AbstractMycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent stu

APA, Harvard, Vancouver, ISO, and other styles

29

Liu, Elizabeth, Yalitza Lopez Corcino, Jose-Andres C. Portillo, Yanling Miao, and Carlos S. Subauste. "Identification of Signaling Pathways by Which CD40 Stimulates Autophagy and Antimicrobial Activity against Toxoplasma gondii in Macrophages." Infection and Immunity 84, no. 9 (2016): 2616–26. http://dx.doi.org/10.1128/iai.00101-16.

Full text

Abstract:

CD40 is an important stimulator of autophagy and autophagic killing ofToxoplasma gondiiin host cells. In contrast to autophagy induced by nutrient deprivation or pattern recognition receptors, less is known about the effects of cell-mediated immunity on Beclin 1 and ULK1, key regulators of autophagy. Here we studied the molecular mechanisms by which CD40 stimulates autophagy in macrophages. CD40 ligation caused biphasic Jun N-terminal protein kinase (JNK) phosphorylation. The second phase of JNK phosphorylation was dependent on autocrine production of tumor necrosis factor alpha (TNF-α). TNF-α

APA, Harvard, Vancouver, ISO, and other styles

30

Jain, Moon, Prasanna K. Sahu, and Kashif Hanif. "Involvement of angiotensin II and beta-adrenergic receptors in the regulation of autophagy in human endothelial EA.hy926 cell line." Tropical Journal of Pharmaceutical Research 19, no. 4 (2020): 751–57. http://dx.doi.org/10.4314/tjpr.v19i4.11.

Full text

Abstract:

Purpose: To investigate the role of angiotensin II (Ang II) and β adrenergic receptors (βARs) in autophagy regulation in human endothelial EA.hy926 cell line.Methods: The effect of pharmacological modulation of Ang II receptors and βARs on the expression of LC3B-II and p62 proteins (autophagosome formation marker and autophagic flux marker, respectively) in the human endothelial EA.hy926 cell line were investigated by immunoblotting technique.Results: Ang II-induced autophagy was characterized by increased LC3B-II and reduced p62 expressions. Candesartan, an AT1R agonist, significantly suppres

APA, Harvard, Vancouver, ISO, and other styles

31

Navarro-Lérida, Inmaculada, Anna M. Aragay, Alejandro Asensio, and Catalina Ribas. "Gq Signaling in Autophagy Control: Between Chemical and Mechanical Cues." Antioxidants 11, no. 8 (2022): 1599. http://dx.doi.org/10.3390/antiox11081599.

Full text

Abstract:

All processes in human physiology relies on homeostatic mechanisms which require the activation of specific control circuits to adapt the changes imposed by external stimuli. One of the critical modulators of homeostatic balance is autophagy, a catabolic process that is responsible of the destruction of long-lived proteins and organelles through a lysosome degradative pathway. Identification of the mechanism underlying autophagic flux is considered of great importance as both protective and detrimental functions are linked with deregulated autophagy. At the mechanistic and regulatory levels, a

APA, Harvard, Vancouver, ISO, and other styles

32

van Niekerk, Gustav, Ashwin W. Isaacs, Theo Nell, and Anna-Mart Engelbrecht. "Sickness-Associated Anorexia: Mother Nature’s Idea of Immunonutrition?" Mediators of Inflammation 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/8071539.

Full text

Abstract:

During an infection, expansion of immune cells, assembly of antibodies, and the induction of a febrile response collectively place continual metabolic strain on the host. These considerations also provide a rationale for nutritional support in critically ill patients. Yet, results from clinical and preclinical studies indicate that aggressive nutritional support does not always benefit patients and may occasionally be detrimental. Moreover, both vertebrates and invertebrates exhibit a decrease in appetite during an infection, indicating that such sickness-associated anorexia (SAA) is evolution

APA, Harvard, Vancouver, ISO, and other styles

33

Niso, Mauro, Joanna Kopecka, Francesca Serena Abatematteo, Francesco Berardi, Chiara Riganti, and Carmen Abate. "Multifunctional thiosemicarbazones targeting sigma receptors: in vitro and in vivo antitumor activities in pancreatic cancer models." Cellular Oncology 44, no. 6 (2021): 1307–23. http://dx.doi.org/10.1007/s13402-021-00638-5.

Full text

Abstract:

Abstract Purpose Association of the metal chelating portion of thiosemicarbazone with the cytotoxic activity of sigma-2 receptors appears a promising strategy for the treatment of pancreatic tumors. Here, we developed a novel sigma-2 receptor targeting thiosemicarbazone (FA4) that incorporates a moiety associated with lysosome destabilization and ROS increase in order to design more efficient antitumor agents. Methods The density of sigma receptors in pancreatic cancer cells was evaluated by flow cytometry. In these cells, cytotoxicity (MTT assay) and activation of ER- and mitochondria-depende

APA, Harvard, Vancouver, ISO, and other styles

34

Furuta, Nobumichi, Naonobu Fujita, Takeshi Noda, Tamotsu Yoshimori, and Atsuo Amano. "Combinational Soluble N-Ethylmaleimide-sensitive Factor Attachment Protein Receptor Proteins VAMP8 and Vti1b Mediate Fusion of Antimicrobial and Canonical Autophagosomes with Lysosomes." Molecular Biology of the Cell 21, no. 6 (2010): 1001–10. http://dx.doi.org/10.1091/mbc.e09-08-0693.

Full text

Abstract:

Autophagy plays a crucial role in host defense, termed antimicrobial autophagy (xenophagy), as it functions to degrade intracellular foreign microbial invaders such as group A Streptococcus (GAS). Xenophagosomes undergo a stepwise maturation process consisting of a fusion event with lysosomes, after which the cargoes are degraded. However, the molecular mechanism underlying xenophagosome/lysosome fusion remains unclear. We examined the involvement of endocytic soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) in xenophagosome/lysosome fusion. Confocal microscopic

APA, Harvard, Vancouver, ISO, and other styles

35

Zientara-Rytter, Katarzyna, and Suresh Subramani. "The Roles of Ubiquitin-Binding Protein Shuttles in the Degradative Fate of Ubiquitinated Proteins in the Ubiquitin-Proteasome System and Autophagy." Cells 8, no. 1 (2019): 40. http://dx.doi.org/10.3390/cells8010040.

Full text

Abstract:

The ubiquitin-proteasome system (UPS) and autophagy are the two major intracellular protein quality control (PQC) pathways that are responsible for cellular proteostasis (homeostasis of the proteome) by ensuring the timely degradation of misfolded, damaged, and unwanted proteins. Ubiquitination serves as the degradation signal in both these systems, but substrates are precisely targeted to one or the other pathway. Determining how and when cells target specific proteins to these two alternative PQC pathways and control the crosstalk between them are topics of considerable interest. The ubiquit

APA, Harvard, Vancouver, ISO, and other styles

36

Noda, Toru, Mary L. Bronson, Shang-Ming Yu, and Marilyn G. Farquhar. "The 215 KD mannose-6-phosphate receptor is involved in crinophagy but not in autophagy." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (1990): 932–33. http://dx.doi.org/10.1017/s0424820100162223.

Full text

Abstract:

Autophagy and crinophagy represent the two major pathways for digestion of intracellular material via lysosomes have been described. Though both phenomena involve in corporation of cell organelles into lysosomes and thus degradation by lysosomal enzymes, the process by which autophagic and crinophagic vacuoles acquire lysosomal enzymes remains to be clarified. The aim of this work is to find out if mannose-6-phosphate (M6P) receptors are involved in this process. As a typical working model, we used hepatocytes of leupeptin-treated rats for autophagy (Fig. 1) and mammotrophs of female rats trea

APA, Harvard, Vancouver, ISO, and other styles

37

Trapannone, Riccardo, Julia Romanov, and Sascha Martens. "p62 and NBR1 functions are dispensable for aggrephagy in mouse ESCs and ESC-derived neurons." Life Science Alliance 6, no. 11 (2023): e202301936. http://dx.doi.org/10.26508/lsa.202301936.

Full text

Abstract:

Accumulation of protein aggregates is a hallmark of various neurodegenerative diseases. Selective autophagy mediates the delivery of specific cytoplasmic cargo material into lysosomes for degradation. In aggrephagy, which is the selective autophagy of protein aggregates, the cargo receptors p62 and NBR1 were shown to play important roles in cargo selection. They bind ubiquitinated cargo material via their ubiquitin-associated domains and tether it to autophagic membranes via their LC3-interacting regions. We used mouse embryonic stem cells (ESCs) in combination with genome editing to obtain fu

APA, Harvard, Vancouver, ISO, and other styles

38

Ding, Wen-Xing, and Xiao-Ming Yin. "Mitophagy: mechanisms, pathophysiological roles, and analysis." Biological Chemistry 393, no. 7 (2012): 547–64. http://dx.doi.org/10.1515/hsz-2012-0119.

Full text

Abstract:

Abstract Mitochondria are essential organelles that regulate cellular energy homeostasis and cell death. The removal of damaged mitochondria through autophagy, a process called mitophagy, is thus critical for maintaining proper cellular functions. Indeed, mitophagy has been recently proposed to play critical roles in terminal differentiation of red blood cells, paternal mitochondrial degradation, neurodegenerative diseases, and ischemia or drug-induced tissue injury. Removal of damaged mitochondria through autophagy requires two steps: induction of general autophagy and priming of damaged mito

APA, Harvard, Vancouver, ISO, and other styles

39

Christ, Maximilian, Heike Huesmann, Heike Nagel, Andreas Kern, and Christian Behl. "Sigma-1 Receptor Activation Induces Autophagy and Increases Proteostasis Capacity In Vitro and In Vivo." Cells 8, no. 3 (2019): 211. http://dx.doi.org/10.3390/cells8030211.

Full text

Abstract:

Dysfunction of autophagy and disturbed protein homeostasis are linked to the pathogenesis of human neurodegenerative diseases and the modulation of autophagy as the protein clearance process has become one key pharmacological target. Due to the role of sigma-1 receptors (Sig-1R) in learning and memory, and the described pleiotropic neuroprotective effects in various experimental paradigms, Sig-1R activation is recognized as one potential approach for prevention and therapy of neurodegeneration and, interestingly, in amyotrophic lateral sclerosis associated with mutated Sig-1R, autophagy is dis

APA, Harvard, Vancouver, ISO, and other styles

40

Liang, Jin Rui, Emily Lingeman, Saba Ahmed, and Jacob E. Corn. "Atlastins remodel the endoplasmic reticulum for selective autophagy." Journal of Cell Biology 217, no. 10 (2018): 3354–67. http://dx.doi.org/10.1083/jcb.201804185.

Full text

Abstract:

Specific receptors are required for the autophagic degradation of endoplasmic reticulum (ER), known as ER-phagy. However, little is known about how the ER is remodeled and separated for packaging into autophagosomes. We developed two ER-phagy–specific reporter systems and found that Atlastins are key positive effectors and also targets of ER-phagy. Atlastins are ER-resident GTPases involved in ER membrane morphology, and Atlastin-depleted cells have decreased ER-phagy under starvation conditions. Atlastin’s role in ER-phagy requires a functional GTPase domain and proper ER localization, both o

APA, Harvard, Vancouver, ISO, and other styles

41

Tan, Tao, Marcel Zimmermann, and Andreas S. Reichert. "Controlling quality and amount of mitochondria by mitophagy: insights into the role of ubiquitination and deubiquitination." Biological Chemistry 397, no. 7 (2016): 637–47. http://dx.doi.org/10.1515/hsz-2016-0125.

Full text

Abstract:

Abstract Mitophagy is a selective autophagy pathway conserved in eukaryotes and plays an essential role in mitochondrial quality and quantity control. Mitochondrial fission and fusion cycles maintain a certain amount of healthy mitochondria and allow the isolation of damaged mitochondria for their elimination by mitophagy. Mitophagy can be classified into receptor-dependent and ubiquitin-dependent pathways. The mitochondrial outer membrane protein Atg32 is identified as the only known receptor for mitophagy in baker’s yeast, whereas mitochondrial proteins FUNDC1, NIX/BNIP3L, BNIP3 and Bcl2L13

APA, Harvard, Vancouver, ISO, and other styles

42

Prick, Tanja, Michael Thumm, Karl Köhrer, Dieter Häussinger, and Stephan Vom Dahl. "In yeast, loss of Hog1 leads to osmosensitivity of autophagy." Biochemical Journal 394, no. 1 (2006): 153–61. http://dx.doi.org/10.1042/bj20051243.

Full text

Abstract:

In mammalian liver, proteolysis is regulated by the cellular hydration state in a microtubule- and p38MAPK (p38 mitogen-activated protein kinase)-dependent fashion. Osmosensing in liver cells towards proteolysis is achieved by activation of integrin receptors. The yeast orthologue of p38MAPK is Hog1 (high-osmolarity glycerol 1), which is involved in the hyperosmotic-response pathway. Since it is not known whether starvation-induced autophagy in yeast is osmosensitive and whether Hog1 is involved in this process, we performed fluorescence microscopy experiments. The hog1Δ cells exhibited a visi

APA, Harvard, Vancouver, ISO, and other styles

43

Vural, Ali, and John H. Kehrl. "Autophagy in Macrophages: Impacting Inflammation and Bacterial Infection." Scientifica 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/825463.

Full text

Abstract:

Macrophages are on the front line of host defense. They possess an array of germline-encoded pattern recognition receptors/sensors (PRRs) that recognize pathogen-associated molecular patterns (PAMPs) and which activate downstream effectors/pathways to help mediate innate immune responses and host defense. Innate immune responses include the rapid induction of transcriptional networks that trigger the production of cytokines, chemokines, and cytotoxic molecules; the mobilization of cells including neutrophils and other leukocytes; the engulfment of pathogens by phagocytosis and their delivery t

APA, Harvard, Vancouver, ISO, and other styles

44

Jimenez-Moreno, Natalia, Carla Salomo-Coll, Laura C. Murphy, and Simon Wilkinson. "Signal-Retaining Autophagy Indicator as a Quantitative Imaging Method for ER-Phagy." Cells 12, no. 8 (2023): 1134. http://dx.doi.org/10.3390/cells12081134.

Full text

Abstract:

Autophagy is an intracellular lysosomal degradation pathway by which cytoplasmic cargoes are removed to maintain cellular homeostasis. Monitoring autophagy flux is crucial to understand the autophagy process and its biological significance. However, assays to measure autophagy flux are either complex, low throughput or not sensitive enough for reliable quantitative results. Recently, ER-phagy has emerged as a physiologically relevant pathway to maintain ER homeostasis but the process is poorly understood, highlighting the need for tools to monitor ER-phagy flux. In this study, we validate the

APA, Harvard, Vancouver, ISO, and other styles

45

Kołodziej, Marta, Panagiotis Tsapras, Alexander D. Cameron, and Ioannis P. Nezis. "Transcription Factor Deformed Wings Is an Atg8a-Interacting Protein That Regulates Autophagy." Cells 13, no. 22 (2024): 1897. http://dx.doi.org/10.3390/cells13221897.

Full text

Abstract:

LC3 (microtubule-associated protein 1 light chain 3, called Atg8 in yeast and Drosophila) is one of the most well-studied autophagy-related proteins. LC3 controls the selectivity of autophagic degradation by interacting with LIR (LC3-interacting region) motifs also known as AIM (Atg8-interacting motifs) on selective autophagy receptors that carry cargo for degradation. Although the function of Atg8 family proteins is primarily cytoplasmic, they are also enriched in the nucleus. Despite the accumulating evidence indicating the presence of Atg8 proteins in the nucleus, the mechanisms by which th

APA, Harvard, Vancouver, ISO, and other styles

46

Kumar, Ravinder, Ankit Shroff, and Taras Y. Nazarko. "Komagataella phaffii Cue5 Piggybacks on Lipid Droplets for Its Vacuolar Degradation during Stationary Phase Lipophagy." Cells 11, no. 2 (2022): 215. http://dx.doi.org/10.3390/cells11020215.

Full text

Abstract:

Recently, we developed Komagataella phaffii (formerly Pichia pastoris) as a model for lipophagy, the selective autophagy of lipid droplets (LDs). We found that lipophagy pathways induced by acute nitrogen (N) starvation and in stationary (S) phase have different molecular mechanisms. Moreover, both types of lipophagy are independent of Atg11, the scaffold protein that interacts with most autophagic receptors and, therefore, is essential for most types of selective autophagy in yeast. Since yeast aggrephagy, the selective autophagy of ubiquitinated protein aggregates, is also independent of Atg

APA, Harvard, Vancouver, ISO, and other styles

47

Sanwald, Julia L., Jochen Dobner, Indra M. Simons, et al. "Lack of GABARAP-Type Proteins Is Accompanied by Altered Golgi Morphology and Surfaceome Composition." International Journal of Molecular Sciences 22, no. 1 (2020): 85. http://dx.doi.org/10.3390/ijms22010085.

Full text

Abstract:

GABARAP (γ-aminobutyric acid type A receptor-associated protein) and its paralogues GABARAPL1 and GABARAPL2 comprise a subfamily of autophagy-related Atg8 proteins. They are studied extensively regarding their roles during autophagy. Originally, however, especially GABARAPL2 was discovered to be involved in intra-Golgi transport and homotypic fusion of post-mitotic Golgi fragments. Recently, a broader function of mammalian Atg8s on membrane trafficking through interaction with various soluble N-ethylmaleimide-sensitive factor-attachment protein receptors (SNAREs) was suggested. By immunostaini

APA, Harvard, Vancouver, ISO, and other styles

48

Santiago-OFarrill, Janice M., Jing Guo, Hailing Yang, Maggie Mao, Zhen Lu, and Robert Bast. "Abstract 2515: DIRAS3 suppresses ovarian cancer cell growth through the inhibition of fibronectin-mediated FAK/AKT signaling." Cancer Research 83, no. 7_Supplement (2023): 2515. http://dx.doi.org/10.1158/1538-7445.am2023-2515.

Full text

Abstract:

Abstract Autophagy is a highly conserved cellular process that maintains homeostasis by degrading and recycling long-lived or misfolded proteins and damaged organelles. In addition, autophagy can protect cells from diverse types of cellular stress produced by amino acid starvation and hypoxia, providing energy to retain the function of organelles and cellular signaling pathways. In cancer, autophagy can play dual roles, inhibiting tumor cell growth and viability or sustaining cancer cells in hypoxic, nutrient poor microenvironments. DIRAS3 (ARHI), a maternally imprinted tumor suppressor gene,

APA, Harvard, Vancouver, ISO, and other styles

49

Mohapatra, Sipra, Tapas Chakraborty, Sonoko Shimizu, Kayoko Ohta, Yoshitaka Nagahama, and Kohei Ohta. "Estrogen and estrogen receptors chauffeur the sex-biased autophagic action in liver." Cell Death & Differentiation 27, no. 11 (2020): 3117–30. http://dx.doi.org/10.1038/s41418-020-0567-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Ylä-Anttila, Päivi. "Autophagy receptors as viral targets." Cellular & Molecular Biology Letters 26, no. 1 (2021). http://dx.doi.org/10.1186/s11658-021-00272-x.

Full text

Abstract:

AbstractActivation of autophagy is part of the innate immune response during viral infections. Autophagy involves the sequestration of endogenous or foreign components from the cytosol within double-membraned vesicles and the delivery of their content to the lysosomes for degradation. As part of innate immune responses, this autophagic elimination of foreign components is selective and requires specialized cargo receptors that function as links between a tagged foreign component and the autophagic machinery. Pathogens have evolved ways to evade their autophagic degradation to promote their rep

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!