Pinelopi Engskog-Vlachos

ORCID: 0009-0004-8205-0200
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Research Areas
  • Cell death mechanisms and regulation
  • Cancer-related Molecular Pathways
  • Epigenetics and DNA Methylation
  • Autophagy in Disease and Therapy
  • Cancer Research and Treatments
  • Microtubule and mitosis dynamics
  • Sirtuins and Resveratrol in Medicine
  • Histone Deacetylase Inhibitors Research
  • Hedgehog Signaling Pathway Studies
  • Inflammasome and immune disorders
  • Cardiomyopathy and Myosin Studies
  • Biochemical effects in animals
  • Ferroptosis and cancer prognosis
  • Polyamine Metabolism and Applications
  • Inflammation biomarkers and pathways
  • interferon and immune responses
  • Genomics, phytochemicals, and oxidative stress
  • Immune cells in cancer
  • Adenosine and Purinergic Signaling
  • Ubiquitin and proteasome pathways
  • Cancer-related gene regulation
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Immune Response and Inflammation
  • Cannabis and Cannabinoid Research
  • Peptidase Inhibition and Analysis

Karolinska Institutet
2005-2023

Abstract Inactivating mutations in the SETD2 gene, encoding for a nonredundant histone H3 methyltransferase and regulator of transcription, is frequent molecular feature clear cell renal carcinomas (ccRCC). deficiency associated with recurrence ccRCC bears low prognostic values. Targeting autophagy, conserved catabolic process critical functions maintenance cellular homeostasis conservation under stress condition, emerging as potential therapeutic strategy to combat ccRCC. Epigenetics-based...

10.1038/s41419-020-2266-x article EN cc-by Cell Death and Disease 2020-01-27

Macroautophagy/autophagy is a conserved catabolic pathway that targets cytoplasmic components for their degradation and recycling in an autophagosome-dependent lysosomal manner. Under physiological conditions, this process maintains cellular homeostasis. However, autophagy can be stimulated upon different forms of stress, ranging from nutrient starvation to exposure drugs. Thus, seen as central component the integrated adaptive stress response. Here, we report even brief induction coupled

10.1080/15548627.2020.1816664 article EN cc-by Autophagy 2020-09-02

Macroautophagy/autophagy is a tightly regulated catabolic process, which contributes at baseline level to cellular homeostasis, and upon its stimulation the adaptive response intra- extracellular stress stimuli. Decrease of autophagy activity occurring aging thought contribute age-related-diseases. Recently, we uncovered, induction, role de novo DNMT3A (DNA methyltransferase 3 alpha)-mediated DNA methylation on expression MAP1LC3 (microtubule associated protein 1 light chain 3) proteins,...

10.1080/15548627.2022.2039993 article EN cc-by Autophagy 2022-02-28

Abstract Caspases are a family of proteins mostly known for their role in the activation apoptotic pathway leading to cell death. In last decade, caspases have been found fulfill other tasks regulating phenotype independently Microglia immune cells brain responsible maintenance physiological functions but can also be involved disease progression when overactivated. We previously described non-apoptotic roles caspase-3 (CASP3) regulation inflammatory microglial or pro-tumoral context tumors....

10.1038/s41419-023-05714-2 article EN cc-by Cell Death and Disease 2023-03-11

Abstract Macroautophagy/autophagy is an evolutionarily conserved and tightly regulated catabolic process involved in the maintenance of cellular homeostasis whose dysregulation implicated several pathological processes. Autophagy begins with formation phagophores that engulf cytoplasmic cargo mature into double-membrane autophagosomes; latter fuse lysosomes/vacuoles for degradation recycling. Here, we report yeast Set2, a histone lysine methyltransferase, its mammalian homolog, SETD2, both...

10.1038/s41419-022-05381-9 article EN cc-by Cell Death and Disease 2022-11-12

The p73 gene, a member of the p53 family, encodes several variants through differential splicing and use alternative promoters. At NH2 terminus, two different promoters generate full-length DeltaN isoforms, with or without transactivating domain. COOH seven isoforms generated have been cloned. Previous studies demonstrated that DeltaNp73 exert dominant-negative effect on by blocking their transactivation activity hence ability to induce apoptosis. Considerable efforts are made identify...

10.1074/jbc.m500394200 article EN cc-by Journal of Biological Chemistry 2005-08-09

p57 (Kip2, cyclin-dependent kinase inhibitor 1C), often found downregulated in cancer, is reported to hold tumor suppressor properties. Originally described as a (cdk) inhibitor, p57KIP2 has since been shown influence other cellular processes, beyond cell cycle regulation, including death and migration. Inhibition of migration by attributed the stabilization actin cytoskeleton through activation LIM domain kinase-1 (LIMK-1). Furthermore, able enhance mitochondrial-mediated apoptosis. Here,...

10.1038/cddis.2012.51 article EN cc-by Cell Death and Disease 2012-05-17

// Maria Jose Oliva-Martin 1,2,3 , Luis Ignacio Sanchez-Abarca 3 Johanna Rodhe 2 Alejandro Carrillo-Jimenez 1 Pinelopi Vlachos Antonio Herrera Albert Garcia-Quintanilla Teresa Caballero-Velazquez Perez-Simon 3,* Bertrand Joseph 2,* and Venero 1,* Department of Biochemistry Molecular Biology, Faculty Pharmacy, Universidad de Sevilla, Spain Oncology-Pathology, Cancer Centrum Karolinska, Karolinska Institutet, Stockholm, Sweden Instituto Biomedicina Sevilla (IBiS)-/CSIC/ * Co-senior authors...

10.18632/oncotarget.9648 article EN Oncotarget 2016-05-26

The transcription factor p73, a member of the p53 family proteins, is involved in regulation cell cycle progression and apoptosis. However, regulatory mechanisms controlling distinct roles for p73 these two processes have remained unclear. Here, we report that able to induce arrest independently its amino-terminal transactivation domain, whereas this domain crucial proapoptotic functions. We also characterized second carboxy terminus within amino acid residues 381 399. This was found...

10.1128/mcb.00585-08 article EN Molecular and Cellular Biology 2009-01-22
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