MIN6 Mouse Insulinoma Cell Line

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.

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.

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