Hmgb1 Knock Out MEF Large T antigen

- Overview
  - Hmgb1 knock out and wild type embryonic fibroblast immortalized with large T antigen
    The knockout cells are generated by the laboratory of Prof. Marco E. Bianchi for research purposes. San Raffaele Research Institute remains the owner of the intellectual property associated to these cells, and requires anyone interested in acquiring them to sign an MTA.
    The cells are shipped in dry ice. Since they are living biological material, they will be checked at customs. Therefore, communication between us and the buyer is required to optimize the delivery.
    
    These are non-syngenic, and derive from a F2 cross of 129Sv and C57Bl/6 mice (Calogero et al. The lack of chromosomal protein HMG1 does not disrupt cell growth, but causes lethal hypoglycaemia in newborn mice. Nature Genet 1999, 22: 276-80).
    
    These lines are called VA1 (Hmgb1 / ) and C1 (Hmgb1-/-). Please be advised that these cells contain HMGB2, which in most instances is redundant to HMGB1. Hmgb1-/- cells grow more slowly than Hmgb1 / cells, and are less resistant to freezing.
    
    Please contact us at for specific academic pricing.
- Properties
  - Categories
    
    Cells
    
    * This product is intended for research only, and cannot be used on humans.
- Reference
  - The elucidation of the anti-inflammatory mechanism of EMO in rheumatoid arthritis through an integrative approach combining bioinformatics and experimental verification
    High-mobility group box-1 peptide ameliorates bronchopulmonary dysplasia by suppressing inflammation and fibrosis in a mouse model
    MIR-107/HMGB1/FGF-2 axis responds to excessive mechanical stretch to promote rapid repair of vascular endothelial cells
    Nucleosome loss facilitates the chemotactic response of macrophages
    Ligand-activated peroxisome proliferator-activated receptor-δ and -γ inhibit lipopolysaccharide-primed release of high mobility group box 1 through upregulation of SIRT1
    Cross-reactivity of anti-HMGB1 antibodies for HMGB2
    Chromatin conformation regulates the coordination between DNA replication and transcription
    Intestinal epithelial HMGB1 inhibits bacterial infection via STAT3 regulation of autophagy
    FSHD muscle shows perturbation in fibroadipogenic progenitor cells, mitochondrial function and alternative splicing independently of inflammation
    A Review of Proposed Mechanisms in Rheumatoid Arthritis and Therapeutic Strategies for the Disease
    Blockade of HMGB1 Reduces Inflammation and Pruritus in Atopic Dermatitis by Inhibiting Skin Fibroblasts Activation
    NOD2 attenuates osteoarthritis via reprogramming the activation of synovial macrophages
    The elucidation of the anti-inflammatory mechanism of EMO in rheumatoid arthritis through an integrative approach combining bioinformatics and experimental verification
    Nucleotide-Binding Oligomerization Domain-Like Receptor 3 Deficiency Attenuated Isoproterenol-Induced Cardiac Fibrosis via Reactive Oxygen Species/High Mobility Group Box 1 Protein Axis
    Extracellular HMGB1 Contributes to the Chronic Cardiac Allograft Vasculopathy/Fibrosis by Modulating TGF-β1 Signaling
    Damage associated molecular pattern molecule-induced microRNAs (DAMPmiRs) in human peripheral blood mononuclear cells
    Autophagy-dependent secretion: mechanism, factors secreted, and disease implications
    HMGB1 modulates the balance between senescence and apoptosis in response to genotoxic stress
    The Association of HMGB1 and RAGE Gene Polymorphisms with IgA Vasculitis
    HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction
    The Anti-inflammatory Effects of HMGB1 Blockades in a Mouse Model of Cutaneous Vasculitis
    Nonoxid-HMGB1 Attenuates Cognitive Impairment After Traumatic Brain Injury in Rats
    Scaffidi et al. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature 2002, 418: 191