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Добірка наукової літератури з теми "CK-1δ"

Автор: Grafiati

Опубліковано: 1 квітня 2023

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Статті в журналах з теми "CK-1δ"

1

Morales-Garcia, José A., Irene G. Salado, Marina Sanz-San Cristobal, Carmen Gil, Ana Pérez-Castillo, Ana Martínez та Daniel I. Pérez. "Biological and Pharmacological Characterization of Benzothiazole-Based CK-1δ Inhibitors in Models of Parkinson’s Disease". ACS Omega 2, № 8 (30 серпня 2017): 5215–20. http://dx.doi.org/10.1021/acsomega.7b00869.

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2

Redenti, Sara, Irene Marcovich, Teresa De Vita, Concepción Pérez, Rita De Zorzi, Nicola Demitri, Daniel I. Perez та ін. "A Triazolotriazine‐Based Dual GSK‐3β/CK‐1δ Ligand as a Potential Neuroprotective Agent Presenting Two Different Mechanisms of Enzymatic Inhibition". ChemMedChem 14, № 3 (15 січня 2019): 310–14. http://dx.doi.org/10.1002/cmdc.201800778.

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3

Rodríguez-Periñán, Guiomar, Ana de la Encarnación, Fermín Moreno, Adolfo López de Munain, Ana Martínez, Ángeles Martín-Requero, Carolina Alquézar, and Fernando Bartolomé. "Progranulin Deficiency Induces Mitochondrial Dysfunction in Frontotemporal Lobar Degeneration with TDP-43 Inclusions." Antioxidants 12, no. 3 (February 25, 2023): 581. http://dx.doi.org/10.3390/antiox12030581.

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Loss-of-function (LOF) mutations in GRN gene, which encodes progranulin (PGRN), cause frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). FTLD-TDP is one of the most common forms of early onset dementia, but its pathogenesis is not fully understood. Mitochondrial dysfunction has been associated with several neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). Here, we have investigated whether mitochondrial alterations could also contribute to the pathogenesis of PGRN deficiency-associated FTLD-TDP. Our results showed that PGRN deficiency induced mitochondrial depolarization, increased ROS production and lowered ATP levels in GRN KD SH-SY5Y neuroblastoma cells. Interestingly, lymphoblasts from FTLD-TDP patients carrying a LOF mutation in the GRN gene (c.709-1G > A) also demonstrated mitochondrial depolarization and lower ATP levels. Such mitochondrial damage increased mitochondrial fission to remove dysfunctional mitochondria by mitophagy. Interestingly, PGRN-deficient cells showed elevated mitochondrial mass together with autophagy dysfunction, implying that PGRN deficiency induced the accumulation of damaged mitochondria by blocking its degradation in the lysosomes. Importantly, the treatment with two brain-penetrant CK-1δ inhibitors (IGS-2.7 and IGS-3.27), known for preventing the phosphorylation and cytosolic accumulation of TDP-43, rescued mitochondrial function in PGRN-deficient cells. Taken together, these results suggest that mitochondrial function is impaired in FTLD-TDP associated with LOF GRN mutations and that the TDP-43 pathology linked to PGRN deficiency might be a key mechanism contributing to such mitochondrial dysfunction. Furthermore, our results point to the use of drugs targeting TDP-43 pathology as a promising therapeutic strategy for restoring mitochondrial function in FTLD-TDP and other TDP-43-related diseases.

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4

Gürbüz, Perihan, Alim Hüseyin Dokumacı, Miyase Gözde Gündüz, Concepcion Perez, Fatih Göger, Mehmet Yavuz Paksoy, Mükerrem Betül Yerer та L. Ömür Demirezer. "In vitro biological activity of Salvia fruticosa Mill. infusion against amyloid β-peptide-induced toxicity and inhibition of GSK-3β, CK-1δ, and BACE-1 enzymes relevant to Alzheimer's disease". Saudi Pharmaceutical Journal 29, № 3 (березень 2021): 236–43. http://dx.doi.org/10.1016/j.jsps.2021.01.007.

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5

Hondius, David C., Frank Koopmans, Conny Leistner, Débora Pita-Illobre, Regina M. Peferoen-Baert, Fenna Marbus, Iryna Paliukhovich, et al. "The proteome of granulovacuolar degeneration and neurofibrillary tangles in Alzheimer’s disease." Acta Neuropathologica 141, no. 3 (January 25, 2021): 341–58. http://dx.doi.org/10.1007/s00401-020-02261-4.

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AbstractGranulovacuolar degeneration (GVD) is a common feature in Alzheimer’s disease (AD). The occurrence of GVD is closely associated with that of neurofibrillary tangles (NFTs) and GVD is even considered to be a pre-NFT stage in the disease process of AD. Currently, the composition of GVD bodies, the mechanisms associated with GVD and how GVD exactly relates to NFTs is not well understood. By combining immunohistochemistry (IHC) and laser microdissection (LMD) we isolated neurons with GVD and those bearing tangles separately from human post-mortem AD hippocampus (n = 12) using their typical markers casein kinase (CK)1δ and phosphorylated tau (AT8). Control neurons were isolated from cognitively healthy cases (n = 12). 3000 neurons per sample were used for proteome analysis by label free LC–MS/MS. In total 2596 proteins were quantified across samples and a significant change in abundance of 115 proteins in GVD and 197 in tangle bearing neurons was observed compared to control neurons. With IHC the presence of PPIA, TOMM34, HSP70, CHMP1A, TPPP and VXN was confirmed in GVD containing neurons. We found multiple proteins localizing specifically to the GVD bodies, with VXN and TOMM34 being the most prominent new protein markers for GVD bodies. In general, protein groups related to protein folding, proteasomal function, the endolysosomal pathway, microtubule and cytoskeletal related function, RNA processing and glycolysis were found to be changed in GVD neurons. In addition to these protein groups, tangle bearing neurons show a decrease in ribosomal proteins, as well as in various proteins related to protein folding. This study, for the first time, provides a comprehensive human based quantitative assessment of protein abundances in GVD and tangle bearing neurons. In line with previous functional data showing that tau pathology induces GVD, our data support the model that GVD is part of a pre-NFT stage representing a phase in which proteostasis and cellular homeostasis is disrupted. Elucidating the molecular mechanisms and cellular processes affected in GVD and its relation to the presence of tau pathology is highly relevant for the identification of new drug targets for therapy.

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6

Joshi, Kopal, Sukriti Goyal, Sonam Grover, Salma Jamal, Aditi Singh, Pawan Dhar та Abhinav Grover. "Novel group-based QSAR and combinatorial design of CK-1δ inhibitors as neuroprotective agents". BMC Bioinformatics 17, S19 (грудень 2016). http://dx.doi.org/10.1186/s12859-016-1379-9.

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7

Martínez-González, Loreto, Carmen Rodríguez-Cueto, Diego Cabezudo, Fernando Bartolomé, Pol Andrés-Benito, Isidro Ferrer, Carmen Gil та ін. "Motor neuron preservation and decrease of in vivo TDP-43 phosphorylation by protein CK-1δ kinase inhibitor treatment". Scientific Reports 10, № 1 (10 березня 2020). http://dx.doi.org/10.1038/s41598-020-61265-y.

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