Table 1 Summary of wild-type and mutant hMLKL properties

From: Conformational switching of the pseudokinase domain promotes human MLKL tetramerization and cell death by necroptosis

hMLKL mutation Location Liposome permeabilization –ATP/+ATP ATP-binding Kd (±SEM; μM) Necroptotic killing function Tumor association
Nil (wild type)   +++/++ 36 ± 4 +
K230M PsK β3 strand ++/++ Delayed K230Q in colon carcinoma
K255A/K256A PsK αC helix +++/++ ND +
E258K PsK αC helix +/+ 24 ± 2 Delayed E258K in colon and endometrial carcinomas19
G330E PsK catalytic loop +/+ 28 ± 6 Delayed G330E melanoma; G330R endometrial carcinoma19
K331N PsK catalytic loop +++/+++ +
E351K PsK activation loop +/++ 26 ± 6 Delayed E351K lung carcinoma19; E351Q prostate adenocarcinoma
K354A/T355A PsK activation loop +++/+++ ND
T357E/S358E PsK activation loop +++/+++ 56 ± 8
K16A/R17A 4HB α1 helix +/+ ND Delayed R17W in endometrial cancer19
D107A/E111A 4HB α4 helix +++/++ 23 ± 2
K157A Brace helices ++/++ 164 ± 31 Delayed
  1. ND not determined; −, not detected