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Journal articles on the topic 'Prenol kinases'

Author: Grafiati

Published: 25 May 2024

Last updated: 31 July 2025

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1

Crispim, Marcell, Ignasi Bofill Verdaguer, Agustín Hernández, et al. "Beyond the MEP Pathway: A novel kinase required for prenol utilization by malaria parasites." PLOS Pathogens 20, no. 1 (2024): e1011557. http://dx.doi.org/10.1371/journal.ppat.1011557.

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A proposed treatment for malaria is a combination of fosmidomycin and clindamycin. Both compounds inhibit the methylerythritol 4-phosphate (MEP) pathway, the parasitic source of farnesyl and geranylgeranyl pyrophosphate (FPP and GGPP, respectively). Both FPP and GGPP are crucial for the biosynthesis of several essential metabolites such as ubiquinone and dolichol, as well as for protein prenylation. Dietary prenols, such as farnesol (FOH) and geranylgeraniol (GGOH), can rescue parasites from MEP inhibitors, suggesting the existence of a missing pathway for prenol salvage via phosphorylation. I

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2

Lee, Miriam, William Wickner, and Hongki Song. "A Rab prenyl membrane-anchor allows effector recognition to be regulated by guanine nucleotide." Proceedings of the National Academy of Sciences 117, no. 14 (2020): 7739–44. http://dx.doi.org/10.1073/pnas.2000923117.

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Membrane fusion is catalyzed by conserved proteins R, Qa, Qb, and Qc SNAREs, which form tetrameric RQaQbQc complexes between membranes; SNARE chaperones of the SM, Sec17/αSNAP, and Sec18/NSF families; Rab-GTPases (Rabs); and Rab effectors. Rabs are anchored to membranes by C-terminal prenyl groups, but can also function when anchored by an apolar polypeptide. Rabs are regulated by GTPase-activating proteins (GAPs), activating the hydrolysis of bound GTP. We have reconstituted fusion with pure components from yeast vacuoles including SNAREs, the HOPS (homotypic fusion and vacuole protein sortin

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3

Qiu, Cong, Yang Liu, Yangbao Wu, Linguo Zhao, and Jianjun Pei. "Functional Characterization and Screening of Promiscuous Kinases and Isopentenyl Phosphate Kinases for the Synthesis of DMAPP via a One-Pot Enzymatic Cascade." International Journal of Molecular Sciences 23, no. 21 (2022): 12904. http://dx.doi.org/10.3390/ijms232112904.

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Dimethylallyl diphosphate (DMAPP) is a key intermediate metabolite in the synthesis of isoprenoids and is also the prenyl donor for biosynthesizing prenylated flavonoids. However, it is difficult to prepare DMAPP via chemical and enzymatic methods. In this study, three promiscuous kinases from Shigella flexneri (SfPK), Escherichia coli (EcPK), and Saccharomyces cerevisiae (ScPK) and three isopentenyl phosphate kinases from Methanolobus tindarius (MtIPK), Methanothermobacter thermautotrophicus str. Delta H (MthIPK), and Arabidopsis thaliana (AtIPK) were cloned and expressed in Escherichia coli.

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Lundquist, Peter K., Anton Poliakov, Lisa Giacomelli, et al. "Loss of Plastoglobule Kinases ABC1K1 and ABC1K3 Causes Conditional Degreening, Modified Prenyl-Lipids, and Recruitment of the Jasmonic Acid Pathway." Plant Cell 25, no. 5 (2013): 1818–39. http://dx.doi.org/10.1105/tpc.113.111120.

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5

Yong, Jun, Shanshan Tang, Lin Yu, Meng Li, Fang Zhang, and Xiujie Fan. "Prenyl diphosphate synthase subunit 2 is downregulated in abdominal aortic aneurysm and retards the progression of abdominal aortic aneurysm." Cytojournal 21 (December 13, 2024): 63. https://doi.org/10.25259/cytojournal_70_2024.

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Objective: Abdominal aortic aneurysm (AAA) is a complex and fatal vascular disease for which specific treatments are still lacking. This study explored the effect and possible mechanisms of prenyl diphosphate synthase subunit 2 (PDSS2) on angiotensin II (Ang II)-induced AAA in human vascular smooth muscle cells (VSMCs). Material and Methods: The AAA cell model was established by treating VSMCs with 1 μM Ang II for 24 h. The effect of Ang II on VSMC viability was detected by cell counting kit-8 assay. The role of PDSS2 on VSMC proliferation was examined using the 5-ethynyl-2'-deoxyuridine metho

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Grant, Benjamin M. M., Masahiro Enomoto, Sung-In Back, et al. "Calmodulin disrupts plasma membrane localization of farnesylated KRAS4b by sequestering its lipid moiety." Science Signaling 13, no. 625 (2020): eaaz0344. http://dx.doi.org/10.1126/scisignal.aaz0344.

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KRAS4b is a small guanosine triphosphatase (GTPase) protein that regulates several signal transduction pathways that underlie cell proliferation, differentiation, and survival. KRAS4b function requires prenylation of its C terminus and recruitment to the plasma membrane, where KRAS4b activates effector proteins including the RAF family of kinases. The Ca2+-sensing protein calmodulin (CaM) has been suggested to regulate the localization of KRAS4b through direct, Ca2+-dependent interaction, but how CaM and KRAS4b functionally interact is controversial. Here, we determined a crystal structure, wh

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7

Wang, Yi-Xuan, Yi-Yuan Jin, Jie Wang, et al. "Icaritin Derivative IC2 Induces Cytoprotective Autophagy of Breast Cancer Cells via SCD1 Inhibition." Molecules 28, no. 3 (2023): 1109. http://dx.doi.org/10.3390/molecules28031109.

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Breast cancer is one of the most prevalent malignancies and the leading cause of cancer-associated mortality in China. Icaritin (ICT), a prenyl flavonoid derived from the Epimedium Genus, has been proven to inhibit the proliferation and stemness of breast cancer cells. Our previous study demonstrated that IC2, a derivative of ICT, could induce breast cancer cell apoptosis by Stearoyl-CoA desaturase 1 (SCD1) inhibition. The present study further investigated the mechanism of the inhibitory effects of IC2 on breast cancer cells in vitro and in vivo. Our results proved that IC2 could stimulate au

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Kollar, Peter, Tomáš Bárta, Stanislava Keltošová, et al. "Flavonoid 4′-O-Methylkuwanon E fromMorus albaInduces the Differentiation of THP-1 Human Leukemia Cells." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/251895.

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Aims. In this work we studied cytodifferentiation effects of newly characterized prenyl flavonoid 4′-O-methylkuwanon E (4ME) isolated from white mulberry (Morus albaL.).Main Methods. Cell growth and viability were measured by dye exclusion assay; cell cycle and surface antigen CD11b were monitored by flow cytometry. For the cytodifferentiation of cells the NBT reduction assay was employed. Regulatory proteins were assessed by western blotting.Key Findings. 4ME induced dose-dependent growth inhibition of THP-1 cells, which was not accompanied by toxic effect. Inhibition of cells proliferation c

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9

Zita, Wayne, Ségolène Bressoud, Gaetan Glauser, Felix Kessler, and Venkatasalam Shanmugabalaji. "Chromoplast plastoglobules recruit the carotenoid biosynthetic pathway and contribute to carotenoid accumulation during tomato fruit maturation." PLOS ONE 17, no. 12 (2022): e0277774. http://dx.doi.org/10.1371/journal.pone.0277774.

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Tomato (Solanum lycopersicum) fruit maturation is associated with a developmental transition from chloroplasts (in mature green fruit) to chromoplasts (in red fruit). The hallmark red color of ripe tomatoes is due to carotenogenesis and accumulation of the red carotenoid lycopene inside chromoplasts. Plastoglobules (PG) are lipid droplets in plastids that are involved in diverse lipid metabolic pathways. In tomato, information on the possible role of PG in carotogenesis and the PG proteome is largely lacking. Here, we outline the role of PG in carotenogenesis giving particular attention to tom

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10

Rocha, Sonia, Daniela Ribeiro, Eduarda Fernandes, and Marisa Freitas. "A Systematic Review on Anti-diabetic Properties of Chalcones." Current Medicinal Chemistry 27, no. 14 (2020): 2257–321. http://dx.doi.org/10.2174/0929867325666181001112226.

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: The use of anti-diabetic drugs has been increasing worldwide and the evolution of therapeutics has been enormous. Still, the currently available anti-diabetic drugs do not present the desired efficacy and are generally associated with serious adverse effects. Thus, entirely new interventions, addressing the underlying etiopathogenesis of type 2 diabetes mellitus, are required. Chalcones, secondary metabolites of terrestrial plants and precursors of the flavonoids biosynthesis, have been used for a long time in traditional medicine due to their wide-range of biological activities, from which

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11

Zayoud, Morad, Einva Vax, Galit Elad Sfadia, Yoel Kloog, and Itamar Goldstein. "Farnesylthiosalicylic acid reduces disease severity in the collagen type-II induced arthritis mouse model by inhibiting Ras Signaling in pathogenic T cells." Journal of Immunology 198, no. 1_Supplement (2017): 224.7. http://dx.doi.org/10.4049/jimmunol.198.supp.224.7.

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Abstract Background Ras proteins are vital for normal T cell activation, and downstream effectors of Ras include the MEK/ERK, PI3-kinase/AKT, and NF-kB pathways. T cells from Rheumatoid Arthritis patients exhibit abnormal activation of the Ras/MEK/ERK pathway. The small molecule Farnesylthiosalicylic acid (FTS) blocks the interaction between Ras proteins and their prenyl binding chaperones, attenuating plasma membrane localization and signaling. Objectives To investigate the immunomodulatory effect of FTS alone or combined with methotrexate (MTX) in the DBA/1 mouse collagen type-II induced art

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12

Benitz, Simone, Malak Nasser, Alexander Steep, et al. "Abstract A109: Single-cell epigenomic analysis reveals an important role of the receptor kinase Ror2 in the erosion of cellular identity during pancreatic carcinogenesis." Cancer Research 84, no. 2_Supplement (2024): A109. http://dx.doi.org/10.1158/1538-7445.panca2023-a109.

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Abstract Introduction The major driver for pancreatic ductal adenocarcinoma (PDAC) is oncogenic KRAS. However, adult acinar cells, a probable origin of PDAC, are largely refractory to KrasG12D-mediated oncogenic transformation. With the concomitant loss of transcription factors that regulate acinar cell differentiation, such as Pdx1 (Pancreatic and Duodenal Homeobox 1), acinar cells undergo a rapid cell identity switch, known as acinar-to-ductal metaplasia (ADM). How loss of cell identity cooperates with oncogenic Kras to induce pancreatic transformation is largely unclear. Methods To elucidat

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Mayer, Ingrid A., Ruth O'Regan, Noah Saul Kornblum, and Kimberly L. Blackwell. "Targeted combination therapy with fulvestrant (FUL) for second-line (2L) treatment of hormone receptor-positive (HR+) advanced breast cancer (ABC)." Journal of Clinical Oncology 35, no. 15_suppl (2017): e12527-e12527. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e12527.

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e12527 Background: FUL is the recommended 2L treatment for patients whose HR+ ABC progressed after aromatase inhibitor (AI) therapy. In first line ABC adding targeted therapy, eg. cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) palbociclib or ribociclib, or mammalian target of rapamycin inhibitor (mTORi) everolimus (EVE), to endocrine therapy (ET) has shown superior efficacy vs ET alone. The use of similar strategies to delay disease progression on ET in the 2L setting is an area of active research. Methods: PubMed and ClinicalTrials.gov were searched for trials investigating FUL + targeted t

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Benitz, Simone, Alec Steep, Malak Nasser, et al. "Abstract C075: Ror2, a Novel Key Regulator Driving Cell Fate Decisions throughout Pancreatic Carcinogenesis." Cancer Research 84, no. 17_Supplement_2 (2024): C075. http://dx.doi.org/10.1158/1538-7445.pancreatic24-c075.

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Abstract Introduction Reprogramming of pancreas cell fate drives development of pancreatic ductal adenocarcinoma (PDAC). Acinar cells, the most probable origin of pancreatic cancer, undergo a rapid cell identity switch towards a duct-like phenotype upon KrasG12D expression and when combined with pancreatitis or the loss of acinar differentiation factors. Metaplastic and neoplastic duct-like cells are heterogeneous with a proportion acquiring features reminiscent of gastric lineages. While some gastric signatures are maintained in the classical PDAC subtype, they are eroded in the more aggressi

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Benitz, Simone, Alexander Steep, Malak Nasser, et al. "Abstract 3939: Ror2, a novel key regulator driving cell fate decisions throughout pancreatic tumor progression." Cancer Research 84, no. 6_Supplement (2024): 3939. http://dx.doi.org/10.1158/1538-7445.am2024-3939.

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Abstract Introduction: Reprogramming of pancreas cell fate drives development of pancreatic ductal adenocarcinoma (PDAC). Acinar cells, the most probable origin of pancreatic cancer, undergo a rapid cell identity switch towards a duct-like phenotype upon KrasG12D expression and when combined with pancreatitis or the loss of acinar differentiation factors. Metaplastic and dysplastic duct-like cells are heterogeneous with a proportion acquiring features reminiscent of gastric lineages. While some gastric signatures are maintained in the classical PDAC subtype, they are eroded in the more aggress

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16

Luger, Selina, Li Chen, Keith W. Pratz, et al. "Gilteritinib Results in Higher Remission and Transplant Rates Than Midostaurin but Does Not Increase the Post-Induction Mutational MRD Negative Rate: Results of the Phase 2 Randomized Precog 0905 Study in Newly Diagnosed FLT3 Mutated AML." Blood 144, Supplement 1 (2024): 221. https://doi.org/10.1182/blood-2024-201595.

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Background: The addition of midostaurin (M), an oral multi-kinase inhibitor, to intensive chemotherapy (IC) prolongs survival in newly diagnosed (ND) FLT3 mutated (m) AML. It is not known if there is a benefit to more potent and selective FLT3 inhibitors. Among these is Gilteritinib (G), now approved as a single agent in relapsed/refractory FLT3m AML. Combined with IC, G also leads to high measurable residual disease (MRD)negative (-) composite complete remission (CRc) in FLT3 Internal Tandem Duplication (ITD)m AML. The aim of the PrECOG 0905 study was to compare FLT3m clearance and CRc rates

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Daver, Naval, Alexander E. Perl, Joseph Maly, et al. "Venetoclax in Combination with Gilteritinib Demonstrates Molecular Clearance of FLT3 mutation in Relapsed/Refractory FLT3-Mutated Acute Myeloid Leukemia." Blood 138, Supplement 1 (2021): 691. http://dx.doi.org/10.1182/blood-2021-150743.

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Abstract Gilteritinib (Gilt), a FLT3 tyrosine kinase inhibitor (TKI), is approved for the treatment of relapsed/refractory (R/R) FLT3-mutated (FLT3 +)acute myeloid leukemia (AML). However, long-term survival is limited by the development of drug resistance mutations in persistent FLT3 + clones. Combination regimens may deepen response and improve outcomes. Venetoclax (Ven), a BCL-2 inhibitor, is approved in combination with hypomethylating agents for newly diagnosed AML not suitable for standard induction therapy. FLT3 + AMLhas been associated with clinical resistance to Ven. Still, FLT3 TKIs

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Altman, Jessica K., Bhavana Bhatnagar, Sameem Abedin, et al. "Gilteritinib Can be Safely Combined with Atezolizumab for the Treatment of Relapsed or Refractory FLT3-Mutated AML: Results of a Phase 1 Study." Blood 138, Supplement 1 (2021): 2343. http://dx.doi.org/10.1182/blood-2021-150707.

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Abstract Background : Gilteritinib, an oral FMS-like tyrosine kinase 3 (FLT3) inhibitor, is approved for the treatment of adults with FLT3-mutated (FLT3mut+) relapsed or refractory (R/R) acute myeloid leukemia (AML) in the United States and many other countries/regions. However, not all respond to treatment and most patients eventually develop recurrent disease. Combining gilteritinib with other agents may improve response. Atezolizumab (840 mg intravenous [IV] every 2 weeks [Q2W]) + azacitidine demonstrated an overall response rate of 62% in hypomethylating agent-naive patients with higher-ri

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Yacoub, Abdulraheem, Uma Borate, Raajit Rampal та ін. "Subgroup Analysis from a Phase 2 Study of the Efficacy and Safety of Parsaclisib, a Selective PI3Kδ Inhibitor, in Combination with Ruxolitinib in Patients with Myelofibrosis (MF)". Blood 138, Supplement 1 (2021): 3647. http://dx.doi.org/10.1182/blood-2021-148668.

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Abstract Background: Despite the demonstrated efficacy of ruxolitinib (potent and selective Janus kinase [JAK] 1 and JAK2 inhibitor) in patients with MF, inadequate responses or loss of response to ruxolitinib may occur, possibly due to persistent activation of the phosphatidylinositol 3-kinase (PI3K) pathway with chronic ruxolitinib therapy. Parsaclisib (INCB050465) is a potent and highly selective next-generation PI3Kδ inhibitor. We previously demonstrated preliminary efficacy in a phase 2 trial (INCB 50465-201, NCT02718300) of parsaclisib added to stable doses of ruxolitinib for patients wi

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Duong, Vu H., Amy S. Ruppert, Alice S. Mims, et al. "Entospletinib (ENTO) and Decitabine (DEC) Combination Therapy in Older Newly Diagnosed (ND) Acute Myeloid Leukemia (AML) Patients with Mutant TP53 or Complex Karyotype Is Associated with Poor Response and Survival: A Phase 2 Sub-Study of the Beat AML Master Trial." Blood 138, Supplement 1 (2021): 1279. http://dx.doi.org/10.1182/blood-2021-151234.

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Abstract Background: In vitro studies and emerging clinical data suggest that inhibition of spleen tyrosine kinase may have an antileukemic effect in human AML. Pts with AML and TP53 mutations (TP53m) are commonly associated with older age (≥60 years) and complex karyotype (CK) and respond poorly to standard 7 + 3 induction (IND) chemotherapy with &lt;10% 1-year overall survival (OS). DEC has been reported to improve response in TP53m AML. Here, we report the results of a Phase 2 sub-study of the Beat AML Master Trial that assessed the efficacy of ENTO + DEC combination treatment (Tx) in N

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Traer, Elie, Ying Huang, Alice S. Mims, et al. "Gilteritinib (GILT) Monotherapy with Addition of Decitabine (DEC) in Non-Responders in Older Newly Diagnosed (ND) FLT3 Mutated Acute Myeloid Leukemia (AML) Patients Having High and Low Variant Allele Frequency (VAF): A Phase 2/1b Sub-Study of the Beat AML Master Trial." Blood 138, Supplement 1 (2021): 1277. http://dx.doi.org/10.1182/blood-2021-148207.

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Abstract Background: GILT is an oral potent selective FLT3 kinase inhibitor approved for marketing for the treatment (Tx) of patients (pts) with relapsed/refractory FLT3 mutated (FLT3m) AML but efficacy in older ND FLT3m AML pts is unknown. Furthermore, FLT3m can be present as a dominant or subclone and impact of FLT3 inhibitor therapy in this setting is uncertain. Here we report the results of a Phase 2/1b sub-study of the Beat AML Master Trial to assess the efficacy of GILT monotherapy (GILTm) in ND FLT3m AML pts aged ≥60 years with high and low VAF and the subsequent response-driven additio

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Cámara Carrillo, Mónica Verenice, Santa Ramírez Godinez, and Juan Carlos Barrera de León. "Prevalencia de rechazo de injerto mediado por anticuerpos en pacientes pediátricos con trasplante renal." Revista de la Sociedad Ecuatoriana de Nefrología, Diálisis y Trasplante 10, no. 2 (2022): 108–14. http://dx.doi.org/10.56867/33.

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Introducción: El objetivo principal en el manejo de los pacientes receptores de trasplante renal, es mantener el estado de inmunosupresión adecuado para evitar la presentación de un rechazo inmunológico del injerto. El rechazo activo mediado por anticuerpos es una de las causas más frecuentes de disfunción del injerto en el periodo postrasplante temprano, además de representar una causa importante de disminución en su sobrevida, sin embargo, en México son escasos los reportes de la prevalencia de este evento, sobre todo en lo referente a la población pediátrica. Métodos: Estudio retrospectivo,

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Alessi, Dario R., and Suzanne R. Pfeffer. "Leucine-Rich Repeat Kinases." Annual Review of Biochemistry, April 15, 2024. http://dx.doi.org/10.1146/annurev-biochem-030122-051144.

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Activating mutations in leucine-rich repeat kinase 2 (LRRK2) represent the most common cause of monogenic Parkinson's disease. LRRK2 is a large multidomain protein kinase that phosphorylates a specific subset of the ∼65 human Rab GTPases, which are master regulators of the secretory and endocytic pathways. After phosphorylation by LRRK2, Rabs lose the capacity to bind cognate effector proteins and guanine nucleotide exchange factors. Moreover, the phosphorylated Rabs cannot interact with their cognate prenyl-binding retrieval proteins (also known as guanine nucleotide dissociation inhibitors)

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24

Jheng, Huei-Fen, Miho Takase, Satoko Kawarasaki, et al. "8-Prenyl daidzein and 8-prenyl genistein from germinated soybean modulate inflammatory response in activated macrophages." Bioscience, Biotechnology, and Biochemistry, April 6, 2023. http://dx.doi.org/10.1093/bbb/zbad041.

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Abstract Soy isoflavones have been shown to have anti-inflammatory properties; however, the anti-inflammatory effects of isoflavone metabolites produced during soybean germination remain unclear. We found that the daidzein and genistein derivatives, 8-prenyl daidzein (8-PD) and 8-prenyl genistein (8-PG), demonstrated a more potent effect than daidzein and genistein on repressing inflammatory responses in macrophages. Although IkB protein levels were unaltered, 8-PD and 8-PG repressed nuclear factor kappa B (NF-κB) activation, which was associated with reduced ERK1/2, JNK, and p38 MAPK activati

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Zhao, Jianli, Jingjing Li, Rui Li, et al. "Abstract 11302: Sevoflurane Pre-Conditioning Effectively Ameliorates Diabetic Myocardial Ischemia/Reperfusion Injury via Differential Regulation of p38 and ERK." Circulation 130, suppl_2 (2014). http://dx.doi.org/10.1161/circ.130.suppl_2.11302.

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Diabetes (DB) significantly exacerbates myocardial ischemia/reperfusion (MI/R) injury. Unfortunately, conventional pre-conditioning (PreCon) provides diminished cardioprotection during DB, due partially to impaired AMP-activated protein kinase (AMPK) signaling. The current study investigated whether PreCon by inhaled anesthetic sevoflurane (SF-PreCon) remains protective in DB, and if so, to dissect the involved mechanisms. Non-diabetic (ND) or high-fat diet-induced DB mice were subjected to MI/R and randomized into control and SF-PreCon (3 cycles of 15 minute-exposures to 2% sevoflurane prior

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Xie, Dina, Jianli Zhao, Rui Guo, et al. "Sevoflurane Pre-conditioning Ameliorates Diabetic Myocardial Ischemia/Reperfusion Injury Via Differential Regulation of p38 and ERK." Scientific Reports 10, no. 1 (2020). http://dx.doi.org/10.1038/s41598-019-56897-8.

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AbstractDiabetes mellitus (DM) significantly increases myocardial ischemia/reperfusion (MI/R) injury. During DM, cardioprotection induced by conventional pre-conditioning (PreCon) is decreased due to impaired AMP-activated protein kinase (AMPK) signaling. The current study investigated whether PreCon with inhaled anesthetic sevoflurane (SF-PreCon) remains cardioprotective during DM, and identified the involved mechanisms. Normal diet (ND) and high-fat diet (HFD)-induced DM mice were randomized into control and SF-PreCon (3 cycles of 15-minute period exposures to 2% sevoflurane) groups before M

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Nazir, Lone A., Naikoo H. Shahid, Kumar Amit, et al. "Synthesis and anti-melanoma effect of 3-O-prenyl glycyrrhetinic acid against B16F10 cells via induction of endoplasmic reticulum stress-mediated autophagy through ERK/AKT signaling pathway." Frontiers in Oncology 12 (August 2, 2022). http://dx.doi.org/10.3389/fonc.2022.890299.

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Melanoma is an aggressive form of cancer with poor prognosis and survival rates and limited therapeutic options. Here, we report the anti-melanoma effect of 3-O-prenyl glycyrrhetinic acid (NPC-402), a derivative of glycyrrhtinic acid, from a reputed medicinal plant Glycyrrhiza glabra against B16F10 cells. We studied the cytotoxic effect of NPC-402 on melanoma cells and investigated the role of mitogen-activated protein (MAP) kinase, AKT axis, and endoplasmic reticulum (ER) stress/unfolded protein response (UPR)-mediated autophagy as the involved signaling cascade by studying specific marker pr

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