Łukasz Samluk

ORCID: 0000-0003-2092-123X
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • Metabolism and Genetic Disorders
  • Amino Acid Enzymes and Metabolism
  • Endoplasmic Reticulum Stress and Disease
  • Drug Transport and Resistance Mechanisms
  • ATP Synthase and ATPases Research
  • Ubiquitin and proteasome pathways
  • Caveolin-1 and cellular processes
  • Alzheimer's disease research and treatments
  • Ion Transport and Channel Regulation
  • Phytochemicals and Antioxidant Activities
  • Cellular transport and secretion
  • Pharmacological Effects and Toxicity Studies
  • Polyamine Metabolism and Applications
  • Protein Kinase Regulation and GTPase Signaling
  • Peroxisome Proliferator-Activated Receptors
  • CRISPR and Genetic Engineering
  • Cholinesterase and Neurodegenerative Diseases
  • Heat shock proteins research
  • Enzyme Structure and Function
  • Redox biology and oxidative stress
  • Ion channel regulation and function
  • Natural product bioactivities and synthesis
  • Essential Oils and Antimicrobial Activity

University of Warsaw
2009-2023

Polish Academy of Sciences
2018-2019

Instytut Biologii Doświadczalnej im. Marcelego Nenckiego
2008-2019

International Institute of Molecular and Cell Biology
2018-2019

The generation of reactive oxygen species (ROS) is inevitably linked to life. However, the precise role ROS in signalling and specific targets largely unknown. We perform a global proteomic analysis delineate yeast redoxome depth more than 4,300 unique cysteine residues over 2,200 proteins. Mapping redox-active thiols proteins exposed exogenous or endogenous mitochondria-derived oxidative stress reveals ROS-sensitive sites several components translation apparatus. Mitochondria are major...

10.1038/s41467-017-02694-8 article EN cc-by Nature Communications 2018-01-16

Abstract Perturbed cellular protein homeostasis (proteostasis) and mitochondrial dysfunction play an important role in neurodegenerative diseases, however, the interplay between these two phenomena remains unclear. Mitochondrial leads to a delay import, causing accumulation of non-imported proteins cytosol challenging proteostasis. Cells respond by increasing proteasome activity molecular chaperones yeast C. elegans . Here, we demonstrate that human cells upregulation chaperone HSPB1 and,...

10.1038/s41467-023-39642-8 article EN cc-by Nature Communications 2023-07-11

Previous studies demonstrated that cells inhibit protein synthesis as a compensatory mechanism for mitochondrial dysfunction. Protein can be attenuated by 1) the inhibition of mTOR kinase, which results in decrease phosphorylation S6K1 and 4E-BP1 proteins, 2) an increase eIF2α protein. The present study investigated both these pathways under conditions short-term acute long-term stress. Short-term responses were triggered mammalian treatment with menadione, antimycin A, or CCCP. Long-term...

10.1091/mbc.e18-10-0628 article EN cc-by-nc-sa Molecular Biology of the Cell 2019-05-22

Accumulating evidence indicates that mitochondrial dysfunction is involved in the pathogenesis of neurodegenerative diseases. Both these conditions are often associated with an increase protein aggregation. However, still unknown specific defects biology play a critical role development Alzheimer's disease, which Tau aggregates observed brains some patients. Here, we report long-term stress triggered dimerization, first step Mitochondrial was induced HEK293T cells received prolonged...

10.1091/mbc.e21-11-0553 article EN Molecular Biology of the Cell 2022-04-21

10.1016/j.bbrc.2012.04.106 article EN Biochemical and Biophysical Research Communications 2012-04-27

OCTN2 - the Organic Cation Transporter Novel family member 2 (SLC22A5) is known to be a xenobiotic/drug transporter. It transports as well carnitine compound necessary for oxidation of fatty acids and mutations its gene cause primary deficiency. Octn2 regulation by protein kinase C (PKC) was studied in rat astrocytes cells which β-oxidation takes place brain. Activation PKC with phorbol ester stimulated L-carnitine transport increased cell surface presence transporter, although no...

10.1371/journal.pone.0082105 article EN cc-by PLoS ONE 2013-12-13

A plasma membrane amino acid transporter B0,+ (ATB0,+), encoded by the SLC6A14 gene, is specific for neutral and basic acids. It up-regulated in several types of malignant cancers. Neurotransmitter transporters SLC6 family interact with SEC24 proteins COPII complex along their pathway from endoplasmic reticulum (ER) to Golgi. This study focused on possible role ATB0,+ trafficking. Rat was expressed HEK293 cells, its localization trafficking were examined Western blot, deglycosylation,...

10.1016/j.bbamcr.2018.11.005 article EN cc-by-nc-nd Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 2018-11-14

Neutral and basic amino acid transporter B(0,+) belongs to a Na,Cl-dependent superfamily of proteins transporting neurotransmitters, acids osmolytes, known be regulated by protein kinase C (PKC). The present study demonstrates an increased phosphorylation on serine moiety after treatment rat astrocytes with phorbol 12-myristate 13-acetate, process correlated augmented activity l-leucine transport enhanced presence the at cell surface. After solubilization Triton X-100 sucrose gradient...

10.1111/j.1471-4159.2010.07040.x article EN Journal of Neurochemistry 2010-10-08

Plasma membrane transporter SLC6A14 transports all neutral and basic amino acids in a Na/Cl – dependent way it is up-regulated many types of cancer. Mass spectrometry analysis overexpressed SLC6A14–associated proteins identified, among others, the presence cytosolic heat shock (HSPs) co-chaperones. We detected co-localization native with HSP90-beta HSP70 (HSPA14). Proximity ligation assay confirmed direct interaction both HSPs. Treatment radicicol VER155008, specific inhibitors HSP90 HSP70,...

10.1016/j.bbamcr.2019.07.009 article EN cc-by-nc-nd Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 2019-07-18

ABSTRACT Perturbed proteostasis and mitochondrial dysfunction are often associated with age-related diseases such as Alzheimer’s Parkinson’s diseases. However, the link between them remains incompletely understood. Mitochondrial causes imbalance, cells respond to restore by increasing proteasome activity molecular chaperons in yeast C. elegans . Here, we demonstrate presence of similar responses humans. upregulates a small heat shock protein HSPB1 an immunoproteasome subunit PSMB9 leading...

10.1101/2021.12.23.473808 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-12-23

Abstract Many studies demonstrated the influence of mitochondrial stress on cytosolic signaling pathways. Here, we found that in cells upon long-term stress, phosphorylation S6K1 protein, which is mTOR pathway component, was increased, like brains Alzheimer’s disease (AD) patients. We checked if increased involved Tau protein aggregation, one AD hallmarks. HEK239T NDUFA11-deficient treatment with inhibitor, INK128, or PF-4708671, caused elevation aggregation. In contrast, stable...

10.1101/2022.06.21.496965 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-06-23
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