Anwarul A. Akhand

TL;DR: It is suggested that progressive dysregulation of the expression level of the ret transgene might play a crucial role in the malignant transformation of melanocytic tumors developed in the MT/ret transgenic mouse line.

TL;DR: Results suggest that the NO/N2O3-provoked S-nitrosylation/S-S bond formation destabilizes the Src structure for Tyr-416 autophosphorylation-associated activation bypassing the Tyr-527-linked regulation.

TL;DR: The results suggest that EGFR may be one of the primary targets of HNE for an oxidative stress-linked cell growth inhibition, and inhibitors prevented HNE-mediated growth inhibition.

TL;DR: It is demonstrated that GO and MGO triggered two distinct signal cascades, one for PTK-dependent control of ERK and another forPTK-independent redox-linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals.

TL;DR: New mechanisms for oxidative stress-mediated PTK activation are suggested including cell-surface glycosylphosphatidylinositol-anchoring proteins and a phosphoglycolipid/cholesterol-enriched membrane microdomain termed a "raft" and intracellular specific cysteine SH groups on PTK proteins can be another target of oxidative stress for inducing a conformational change necessary for initial activation of PTKs.