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Myocardin-related transcription factors (MRTFs: myocardin/MYOCD, MRTF-A/MRTFA, and MRTF-B/MRTFB) are co-factors of serum response factor (SRF) that activate the smooth muscle cell (SMC) gene program and that play roles in cardiovascular development and mechanobiology. Gain and loss of function experiments have defined the SMC gene program under control of MRTFs, yet full understanding of their imp
Senior lecturer Contact details Email: charlotta [dot] nilsson [at] fysik [dot] lu [dot] seOrganisation Particle and nuclear physics Visiting address: Professorsgatan 1, Lund Service point: 14 WebpageCharlotta Nilssons profile in Lund University research portalOther affiliations Member of Strategic Research Area NanoLund: Centre for Nanoscience Profile area member LTH Profile Area: Nanoscience and
https://www.particle-nuclear.lu.se/charlotta-nilsson - 2026-07-16
The processes that govern human haematopoietic stem cell (HSC) self-renewal and engraftment are poorly understood and challenging to recapitulate in culture to reliably expand functional HSCs1–3. Here we identify MYC target 1 (MYCT1; also known as MTLC) as a crucial human HSC regulator that moderates endocytosis and environmental sensing in HSCs. MYCT1 is selectively expressed in undifferentiated
Chromosomal aneuploidy, that is, numerical chromosome aberrations, is one of the molecular hallmarks of cancer. However, when neoplasms are studied with sequencing- and array-based approaches, chromosome numbers and ploidy states are typically inferred from bulk DNA data. Furthermore, published molecular estimates of neoplasia-associated aneuploidy often also include genomic imbalances resulting f
Changes in gene regulation and expression govern orderly transitions from hematopoietic stem cells to terminally differentiated blood cell types. These transitions are disrupted during leukemic transformation, but knowledge of the gene regulatory changes underpinning this process is elusive. We hypothesized that identifying core gene regulatory networks in healthy hematopoietic and leukemic cells
Neoantigens are now recognized drivers of the antitumor immune response. Recurrent neoantigens, shared among groups of patients, have thus become increasingly coveted therapeutic targets. Here, we report on the data-driven identification of a robustly presented, immunogenic neoantigen that is derived from the combination of HLA-A*01:01 and RAS.Q61K. Analysis of large patient cohorts indicated that
Classical conditioning of motor responses, e.g., the eyeblink response, depends on the cerebellum. In the theoretical works of David Marr (1969) and James Albus (1971), it was proposed that Purkinje cells in the cerebellar cortex learn to associate the neutral conditioned stimulus with the response. Since their work, several studies have provided data that are consistent with this suggestion, but
Alexander disease (AxD) is a rare and severe neurodegenerative disorder caused by mutations in glial fibrillary acidic protein (GFAP). While the exact disease mechanism remains unknown, previous studies suggest that mutant GFAP influences many cellular processes, including cytoskeleton stability, mechanosensing, metabolism, and proteasome function. While most studies have primarily focused on GFAP
Marta Pertegás SenderProfessor Marta Pertegás Sender, University of Maastricht, began her career in academia as a doctoral student in Leuven and she defended her thesis on cross-border patent infringement in 2000. As a recent PhD, Marta worked as a teacher and researcher at the University of Antwerp. From 2008 to 2017, she was a permanent member of the Secretariat of the Hague Conference on Privat
https://www.law.lu.se/honorary-doctorates-2025 - 2026-07-15
The tumor microenvironment (TME) is composed of various cellular components such as tumor cells, stromal cells including fibroblasts, adipocytes, mast cells, lymphatic vascular cells and infiltrating immune cells, macrophages, dendritic cells and lymphocytes. The intricate interplay between these cells influences tumor growth, metastasis and therapy failure. Significant advancements in breast canc
In humans, beta-alanine (BAL) and the neurotransmitter gamma-aminobutyrate (GABA) are transaminated by a single aminotransferase enzyme. Apparently, yeast originally also had a single enzyme, but the corresponding gene was duplicated in the Saccharomyces kluyveri lineage. SkUGA1 encodes a homologue of Saccharomyces cerevisiae GABA aminotransferase, and SkPYD4 encodes an enzyme involved in both BAL
Tyrosine kinase inhibitors targeting the BCR-ABL oncoprotein in chronic myeloid leukemia (CML) are remarkably effective inducing deep molecular remission in most patients. However, they are less effective to eradicate the leukemic stem cells (LSC), resulting in disease persistence. Therefore, there is great need to develop novel therapeutic strategies to specifically target the LSC. In an experime
1 CLASSICS IN SPATIAL THEORY PhD course within the Swedish National Program for Research Education in Human Geography, 7,5 ECTS Spring semester 2021 Course Organizers Mekonnen Tesfahuney, Professor, Karlstad University (mete@kau.se), course convener Tomas Germundsson, Professor, Lund University (tomas.germundsson@keg.lu.se) Richard Ek, Associate Professor, Karlstad University (richard.ek@kau.se) S
https://www.keg.lu.se/sites/keg.lu.se/files/classics_in_spatial_theory_phd_course_2021.pdf - 2026-07-17
Cell-based therapies hold great promise in re-establishing organ function for many diseases, including untreatable lung diseases such as idiopathic pulmonary fibrosis (IPF). However, many hurdles still remain, in part due to our lack of knowledge about the disease-driving mechanisms that may affect the cellular niche and thereby possibly hinder the function of any transplanted cells by imposing th
Nicotinamide adenine dinucleotide phosphate (NADPH) enhances Ca(2+)-induced exocytosis in pancreatic beta-cells, an effect suggested to involve the cytosolic redox protein glutaredoxin-1 (GRX-1). We here detail the role of GRX-1 in NADPH-stimulated beta-cell exocytosis and glucose-stimulated insulin secretion. Silencing of GRX-1 by RNA interference reduced glucose-stimulated insulin secretion in b
