A5076996836- Ubiquitin and proteasome pathways
- NF-κB Signaling Pathways
- Microtubule and mitosis dynamics
- Epigenetics and DNA Methylation
- Cancer-related Molecular Pathways
- Cell Adhesion Molecules Research
- Cell death mechanisms and regulation
- Histone Deacetylase Inhibitors Research
- Immunotherapy and Immune Responses
- Neuroblastoma Research and Treatments
- Cancer-related gene regulation
- Cancer Cells and Metastasis
- Cancer, Hypoxia, and Metabolism
- Wnt/β-catenin signaling in development and cancer
- RNA modifications and cancer
- Peptidase Inhibition and Analysis
- Asthma and respiratory diseases
- Inflammatory mediators and NSAID effects
- Immune Response and Inflammation
- Signaling Pathways in Disease
- Cytokine Signaling Pathways and Interactions
- interferon and immune responses
- Cellular Mechanics and Interactions
- Immune Cell Function and Interaction
- Cancer and Skin Lesions
Lund University
2016-2025
Medicon Village
2014-2024
Skåne University Hospital
2011
Max Planck Institute of Biochemistry
2006-2010
Max Planck Society
2006-2010
Malmö University
2001-2010
Taipei Institute of Pathology
2010
High malignancy and early metastasis are hallmarks of melanoma. Here, we report that the transcription factor Snail1 inhibits expression tumor suppressor CYLD in As a direct consequence repression, protooncogene BCL-3 translocates into nucleus activates Cyclin D1 N-cadherin promoters, resulting proliferation invasion melanoma cells. Rescue cells reduced vitro growth vivo. Analysis tissue microarray with primary melanomas from patients revealed an inverse correlation induction loss...
CYLD was originally identified as a tumor suppressor that is mutated in familial cylindromatosis. Recent studies suggested role for nuclear factor-kappaB (NF-κB) regulation. NF-κB activation has been connected with multiple aspects of oncogenesis but the underlying molecular mechanisms persistent tumors remain largely unknown. Thus, we evaluated transcription different colon and hepatocellular carcinoma cell lines tissue samples, respectively. downregulated or lost all investigated compared...
Abstract Microtubule nucleation requires the γ-tubulin ring complex, and during M-phase (mitosis) this complex accumulates at centrosome to support mitotic spindle formation. The posttranslational modification of through ubiquitination is vital for regulating microtubule duplication. Blocking BRCA1/BARD1-dependent causes amplification. In current study, we identified BRCA1-associated protein-1 (BAP1) as a deubiquitination enzyme γ-tubulin. BAP1 was downregulated in metastatic adenocarcinoma...
B cell homeostasis is regulated by multiple signaling processes, including nuclear factor-κB (NF-κB), BAFF-, and receptor signaling. Conditional disruption of genes involved in these pathways has shed light on the mechanisms governing from surface to nucleus. We describe a novel mouse strain that expresses solely excessively naturally occurring splice variant CYLD (CYLDex7/8 mice), which deubiquitinating enzyme integral NF-κB This shorter protein lacks TRAF2 NEMO binding sites present...
Posttranslational modification of different proteins via direct ubiquitin attachment is vital for mediating various cellular processes. Cylindromatosis (CYLD), a deubiquitination enzyme, able to cleave the polyubiquitin chains from substrate and regulate signaling pathways. Loss, or reduced expression, CYLD observed in types human cancer, such as hepatocellular carcinoma (HCC). However, molecular mechanism by which affects cancerogenesis has date not been unveiled. The aim present study was...
Tumors are phenotypically heterogeneous and include subpopulations of cancer cells with stemlike properties. The natural product salinomycin, a K+-selective ionophore, was recently found to exert selectivity against such stem cells. This selective effect is thought be due inhibition the Wnt signaling pathway, but mechanistic basis remains unclear. Here, we develop functionally competent fluorescent conjugate salinomycin investigate molecular mechanism this compound. By subcellular imaging,...
Abstract Background and Purpose Malignant melanoma is the most lethal form of skin cancer, characterised by a poor survival rate. One key factors driving aggressive growth cells elevated expression proto‐oncogene Bcl‐3. This study aims to optimise, evaluate characterise second‐generation Bcl‐3 inhibitor, using as model demonstrate its potential therapeutic efficacy. Experimental Approach We synthesised screened series structural analogues selected A27, promising candidate for further...
By keeping activation of the kinase p38α in check, ubiquitin ligase Itch inhibits skin inflammation mice.
BRCA1-associated protein 1 (BAP1) is a nuclear deubiquitinating enzyme that associated with multiprotein complexes regulate key cellular pathways, including cell cycle, differentiation, death, and the DNA damage response. In this study, we found reduced expression of BAP1 pro6motes survival neuroblastoma cells, restoring levels in these cells facilitated delay S G2/M phase as well apoptosis. The mechanism induces death mediated via an interaction 14-3-3 protein. association between releases...
Abstract Molecular targeted therapy using a drug that suppresses the growth and spread of cancer cells via inhibition specific protein is foundation precision medicine treatment. High expression proto-oncogene Bcl-3 promotes proliferation metastasis originating from tissues such as colon, prostate, breast, skin. The development novel drugs targeting alone or in combination with other therapies can cure these patients prolong their survival. As proof concept, present study, we focused on...
Hepatic fibrosis is considered as a physiological wound-healing response to liver injury. The process involves several factors, such hepatocyte growth factor (HGF), which restrains hepatic injury and facilitates reversibility of fibrotic reaction in an acute insult. Chronic sustained inflammation cause progressive and, ultimately, organ dysfunction. mechanisms tipping the balance from restoration tissue scarring are not well understood. In present study, we identify mechanism...