MIN6 Mouse Insulinoma Cell Line

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The MIN6 cell line is a long-term stable mouse pancreatic beta-cell line that retains characteristics of mature β-cells and can be used to analyze insulin secretion/sensitivity in diabetes research.

The Mouse Insulinoma Cell Line (MIN6), was derived from an insulinoma tissue that developed in a transgenic mouse in which the expression of the Simian Virus 40 Large T antigen was driven by the human insulin promoter.^1,2,3 In comparison to the primary pancreatic b-cells, MIN6 thrives reliably and far more robustly in cell culture and yet retains the important characteristics of the b-cells, such as the exclusive expression of the so-called “liver-type” glucose transporter (Glut2) and their ability to modulate the insulin secretion in response to the changing glucose concentration in the growth medium, and it has been a staple strain in diabetes research since its establishment in 1990.

Additionally, the expression of the major histocompatibility complex I (MHC I) is lacking in MIN6, as in the non-diabetic b-cells, but can be induced by pro-inflammatory cytokines,^1,4,5 which would render them susceptible to T-cell mediated cytotoxicity. This closely mimics the behavior of the b-cells isolated from diabetic tissues, where chronic inflammation is commonly observed, and it has made MIN6 an attractive cell line model for investigating the mechanism of the b-cells loss due to their autoimmune destruction.

References
1. Miyazaki J, Araki K, Yamato E, Ikegami H, Asano T, Shibasaki Y, Oka Y, Yamamura K. 1990. Establishment of a pancreatic beta cell line that retains glucose-inducible insulin secretion: special reference to expression of glucose transporter isoforms. Endocrinology. 27(1):126-32.
2. Sarvetnick N, Liggitt D, Pitts SL, Hansen SE, Stewart TA. 1988. Insulin-dependent diabetes mellitus induced in transgenic mice by ectopic expression of class II MHC and interferon-gamma. Cell. 52(5):773-82. Pytynia KB, Dahlstrom KR, Sturgis EM. 2014. Epidemiology of HPV-associated oropharyngeal cancer. Oral Oncol. 50(5): 380-6.
3. Ullrich A, Dull TJ, Gray A, Philips JA 3rd, Peter S. 1982. Variation in the sequence and modification state of the human insulin gene flanking regions. Nucleic Acids Res. 10(7):2225-40.
4. Jiang H, Li Y, Shen M, Liang Y, Qian Y, Dai H, Xu K, Xu X, Lv H, Zhang J, Yang T, Fu Q. 2022. Interferon-α promotes MHC I antigen presentation of islet α cells through STAT1-IRF7 pathway in type 1 diabetes. Immunology. 166(2):210-221.
5. Javeed N, Her TK, Brown MR, Vanderboom P, Rakshit K, Egan AM, Vella A, Lanza I, Matveyenko AV. 2021. Pro-inflammatory α cell small extracellular vesicles induce α cell failure through activation of the CXCL10/CXCR3 axis in diabetes. Cell Rep. 36(8):109613.

This product is intended for sale and sold solely to academic institutions for internal academic research use per the terms of the “Academic Use Agreement” as detailed in the product documentation. For information regarding any other use, please contact licensing@emdmillipore.com.

The cells should be stored in liquid nitrogen. The cells can be cultured for at least 10 passages after initial thawing without significantly affecting the cell marker expression and functionality.