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doi: 10.1210/en.2006-1285

Given that RIPK1 is also integral to the progression of these diseases, we propose the hypothesis that HK2 may regulate RIPK1 via its non-metabolic functions, thereby influencing the progression of cell death

We found that NF-B and MAPK pathways were unaffected by HK2 knockout, as determined by the levels of proteins involved in these pathways and the nuclear translocation of p65 (Supplementary Fig