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2025.03.20 22:04

[HMG Biotech 공식 대리점]Hmgb1knock out and HMGB2 low content MEF with 3T3 method [HM-223]

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Hmgb1knock out and HMGB2 low content MEF with 3T3 method [HM-223]


SKU: HM-223 Categories: Cells, Hmgb1 knock out mouse embryonic fibroblasts 

Tags: HMGB1, HMGB1 Fibroblasts -/- and +/+, Hmgb1-/- MEF

Hmgb1 knock out embryonic fibroblasts immortalized with the 3T3 method, low content of HMGB2 [HM-223]


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.


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.


This immortalized clone of Hmgb1-/- MEFs contains a reduced amount of HMGB2.

This clone was obtained from a cross of Hmgb1 heterozygotes on a pure BALB/c genetic background (>10 backcrosses), 

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.

As wild type controls for these MEFs, we suggest to use the wild type HM-221 MEFs, that will be provided by default with this order.


Publications:

1.The elucidation of the anti-inflammatory mechanism of EMO in rheumatoid arthritis through an integrative approach 

combining bioinformatics and experimental verification

2.High-mobility group box-1 peptide ameliorates bronchopulmonary dysplasia by suppressing inflammation and fibrosis 

in a mouse model

3.MIR-107/HMGB1/FGF-2 axis responds to excessive mechanical stretch to promote rapid repair of vascular endothelial cells

4.Nucleosome loss facilitates the chemotactic response of macrophages

5.Ligand-activated peroxisome proliferator-activated receptor-δ and -γ inhibit lipopolysaccharide-primed release of high 

mobility group box 1 through upregulation of SIRT1

6.Cross-reactivity of anti-HMGB1 antibodies for HMGB2

7.Chromatin conformation regulates the coordination between DNA replication and transcription

8.Intestinal epithelial HMGB1 inhibits bacterial infection via STAT3 regulation of autophagy

9.FSHD muscle shows perturbation in fibroadipogenic progenitor cells, mitochondrial function and alternative 

splicing independently of inflammation

10.A Review of Proposed Mechanisms in Rheumatoid Arthritis and Therapeutic Strategies for the Disease

11.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

12.The elucidation of the anti-inflammatory mechanism of EMO in rheumatoid arthritis through an integrative approach 

combining bioinformatics and experimental verification

13.Nucleotide-Binding Oligomerization Domain-Like Receptor 3 Deficiency Attenuated Isoproterenol-Induced Cardiac 

Fibrosis via Reactive Oxygen Species/High Mobility Group Box 1 Protein Axis

14.Extracellular HMGB1 Contributes to the Chronic Cardiac Allograft Vasculopathy/Fibrosis by Modulating TGF-β1 Signaling

15.Damage associated molecular pattern molecule-induced microRNAs (DAMPmiRs) in human peripheral blood mononuclear cells

16.Autophagy-dependent secretion: mechanism, factors secreted, and disease implications

17.HMGB1 modulates the balance between senescence and apoptosis in response to genotoxic stress

18.The Association of HMGB1 and RAGE Gene Polymorphisms with IgA Vasculitis

19.HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction

20.The Anti-inflammatory Effects of HMGB1 Blockades in a Mouse Model of Cutaneous Vasculitis

21.Nonoxid-HMGB1 Attenuates Cognitive Impairment After Traumatic Brain Injury in Rats

22.Urbonaviciute  et al. (2008) Induction of inflammatory and immune responses by HMGB1-nucleosome complexes – 

implications for the pathogenesis of SLE. J Exp Med 205: 3007-18

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