Hmgb2 knock out mouse embryonic fibroblasts [HM-251]
HMGBiotech distributes the knockout cells 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. Please send a mail to info@hmgbiotech.eu for MTA processing.
The cells are shipped in dry ice. Since they are living biological material, they will be checked at customs. Therefore, communication between HMGBiotech and the buyer is required to optimize the delivery.
These Hmgb2 / and Hmgb2-/- MEFs were obtained from sib embryos from crosses of Hmgb2 heterozygotes (Ronfani et al., Development 128: 1265-73) on a pure BALB/c genetic background (>10 backcrosses, unpublished), and grown according to the 3T3 protocol, which prescribes splitting 1:3 the growing cells every 3 days for 3 months.
We suggest to split the cells, by trypsinization, when they reach 80% confluence.
Publications:
- 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
- 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