Pancreatic Beta Cell Death: Novel Potential Mechanisms in Diabetes Therapy

Figure 1

Apoptosis: the union of ligand IL1-1β, Fas-L, and TNF-α triggers a series of intracelular signals that end with caspase activation, which is capable of mediating the rupture of other proteins in aspartate residues through its cysteine residue (see text). IL-1β: interleukin 1 beta; Fas-L: Fas ligand; TNF-α: tumor necrosis factor alpha; IL-1R1: interleukin 1 receptor type 1; TNFR-1: tumor necrosis factor receptor 1; DD: death domain; TOLLIP: Toll-interacting protein; IL-1 ACP: interleukin 1 receptor accessory protein; MyD88: myeloid differentiation protein; IRAK1: interleukin 1 receptor-associated kinase 1; IRAK4: interleukin 1 receptor-associated kinase 4; TRAF6: TNF receptor-associated factor 6; NEMO: nuclear factor kappa B essential modulator; IKK: inhibitor of nuclear factor kappa B kinase; IKB: NF-κB inhibitor; NF-κB: nuclear factor kappa B; PDX1: insulin promoter factor 1; CHOP: CCAAT enhancer-binding protein homologous protein; iNOS: inducible nitric oxide syntase; ICAD: inhibitor of caspase-activated DNase; PARP: poly ADP-ribose polymerase; RIP1: receptor-interacting protein kinase 1; TRADD: tumor necrosis factor receptor type 1-associated death domain protein; TRAF2: TNF receptor-associated factor 2; DISC: death induction signaling complex; LAMA: laminin A; ACT: actin.