Malin Samuelsson

ORCID: 0000-0002-1337-5288
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About
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Research Areas
  • Alzheimer's disease research and treatments
  • Cell Adhesion Molecules Research
  • NF-κB Signaling Pathways
  • Immune Response and Inflammation
  • Neuroinflammation and Neurodegeneration Mechanisms
  • GDF15 and Related Biomarkers
  • Social and Educational Sciences
  • Molecular Sensors and Ion Detection
  • Botany and Plant Ecology Studies
  • Cellular transport and secretion
  • Light effects on plants
  • Galectins and Cancer Biology
  • Caveolin-1 and cellular processes
  • Mitochondrial Function and Pathology
  • Obesity and Health Practices
  • Atherosclerosis and Cardiovascular Diseases
  • RNA regulation and disease
  • Pharmacological Effects of Natural Compounds
  • RNA Interference and Gene Delivery
  • Education, Healthcare and Sociology Research
  • Signaling Pathways in Disease
  • Photoreceptor and optogenetics research
  • Occupational Therapy Practice and Research
  • Plant responses to elevated CO2
  • Forest Ecology and Biodiversity Studies

Lund University
2016-2019

Stockholm University
2005-2011

University of Gothenburg
2004

Integrins are heterodimeric transmembrane proteins that play a fundamental role in the migration of leukocytes to sites infection or injury. We found protein tyrosine phosphatase nonreceptor type 22 (PTPN22) inhibits signaling by integrin lymphocyte function-associated antigen-1 (LFA-1) effector T cells. PTPN22 colocalized with its substrates at leading edge cells migrating on surfaces coated LFA-1 ligand intercellular adhesion molecule-1 (ICAM-1). Knockout knockdown expression autoimmune...

10.1126/scisignal.aaf2195 article EN Science Signaling 2016-10-04

Abstract Background The transcription factors CCAAT/enhancer binding proteins (C/EBP) α, β and δ have been shown to be expressed in brain involved regulation of inflammatory genes concert with nuclear factor κB (NF-κB). In general, C/EBPα is down-regulated, whereas both C/EBPβ are up-regulated response stimuli. Alzheimer's disease (AD) one the hallmarks chronic neuroinflammation mediated by astrocytes microglial cells, most likely induced formation amyloid-β (Aβ) deposits. AD has ascribed...

10.1186/1742-2094-8-34 article EN cc-by Journal of Neuroinflammation 2011-04-14

Imaging analysis reveals a mechanism for the integrin recycling required to maintain T cell migration.

10.1126/scisignal.aai8629 article EN Science Signaling 2017-12-12

An increasing body of evidence suggests that β-amyloid (Aβ) and activated glial cells play a crucial part in the pathogenesis Alzheimer's disease (AD). Activated surrounding senile plaques, formed by Aβ peptides, have been proposed to promote neurodegeneration producing putatively toxic factors, including inflammatory cytokine interleukin-1β (IL-1β). Elevated levels both IL-1β nuclear factor κB (NF-κB), key transcription regulating wide variety genes, found brains AD patients. In this study,...

10.3892/ijmm.16.3.449 article EN International Journal of Molecular Medicine 2005-09-01

Abstract Background Recent studies indicate local caspase activation in dendrites or axons during development and neurodegenerative disorders such as Alzheimer's disease (AD). Emerging evidences point to soluble oligomeric amyloid-β peptide a causative agent AD. Results Here we describe the design of fluorescence resonance energy transfer (FRET)-based sensors, fused microtubule associated protein tau. Specific sensors preferentially cleaved by caspase-3, -6 -9 were expressed differentiated...

10.1186/1750-1326-6-35 article EN cc-by Molecular Neurodegeneration 2011-05-23

To enable cells to move forward, cell surface integrins are internalized into an endosomal compartment and subsequently intracellularly transported be re-exposed at a new site on the membrane. Leukocytes fastest migrating type in human body, which express leukocyte-specific integrin LFA-1. Here, we describe flow cytometry-based assay that allows quantification of LFA-1 internalization its re-expression T lymphocytes. An advantage using over biochemical methods is low number needed cells....

10.21769/bioprotoc.3104 article EN BIO-PROTOCOL 2018-01-01

Chronic neuroinflammation is believed to play a role in Alzheimer's disease (AD). Evidence indicates that the transcription factor CCAAT/enhancer binding protein (C/EBP) family involved inflammatory mechanisms during AD. Many genes can be regulated by C/EBP, including encoding IL-1, IL-6 and TNFα. It has also been shown C/EBPβ δ are overexpressed Expression of induced stimuli glial cells, whereas C/EBPα expression inhibited. Our group previously dysregulation C/EBP activity following...

10.1016/j.jalz.2010.05.872 article EN Alzheimer s & Dementia 2010-07-01

To be able to migrate, leukocyte needs re-use its adhesion molecules move forward. These are called integrins and intracellularly transported via endocytosis exocytosis in order translocate a new site on the cell membrane. The intracellular transportation is regulated by different small GTPases including RhoB. Here we describe an activation assay of RhoB leukocytes migrating ICAM-1Fc coated dishes using commercially available Rhoteikin agarose beads. Although this specific protocol for LFA-1...

10.21769/bioprotoc.3105 article EN BIO-PROTOCOL 2018-01-01

Neuronal and synaptic loss can be observed in several neurologic disorders, like Alzheimer's disease (AD). The mechanism behind cell death AD has been intensively studied apoptosis proposed to play a central role processes, primary affecting cholinergic neurons the cerebral cortex limbic lobe. There are numerous potential stimuli that may relevant AD, including inflammatory responses, growth factor deprivation, oxidative stress direct effects of β– amyloid peptide. In order get further...

10.1016/j.jalz.2006.05.1488 article EN Alzheimer s & Dementia 2006-07-01

Accumulating evidence supports the importance of inflammation in neurodegenerative disorders like Alzheimer's disease (AD). Epidemiological studies have revealed that patients taking anti–inflammatory drugs for conditions arthritis a lower prevalence than others. In addition, there are reports show indeed can cause neurodegeneration vivo. “The glial loop hypothesis” describes model where surrounding cells activated and produce neurotoxic products therefore lead to neuronal death. One most...

10.1016/j.jalz.2006.05.1547 article EN Alzheimer s & Dementia 2006-07-01
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