The monoclonal antibody EPR1614Y against the stem cell biomarker keratin K15 lacks specificity and reacts with other keratins.

Keratin 15 (K15), a type I keratin, which pairs with K5 in epidermis, has been used extensively as a biomarker for stem cells. Two commercial antibodies, LHK15, a mouse monoclonal and EPR1614Y, a rabbit monoclonal, have been widely employed to study K15 expression. Here we report differential reactivity of these antibodies on epithelial cells and tissue sections.

The mitochondrial effects of embelin are independent of its MAP kinase regulation: Role of p53 in conferring selectivity towards cancer cells.

Amongst various therapeutic properties of the natural product embelin, its anti-cancer effects are being extensively studied. We observed that, embelin induced apoptosis in A549 cells lacking functional mitochondria (ρ0 cells) indicating that its mitochondrial effects are not primarily responsible for its anti-cancer activity. However, p38 mediated activation of p53 was found to play a pivotal role in governing the apoptotic activity of embelin due to the following observations: a time-dependent activation of p53 and apoptosis by embelin; selective inhibition of p38 inhibited embelin-induced p53 levels.

NOD2 activation induces oxidative stress contributing to mitochondrial dysfunction and insulin resistance in skeletal muscle cells.

Nucleotide-binding oligomerization domain protein-2 (NOD2) activation in skeletal muscle cells has been associated with insulin resistance, but the underlying mechanisms are not yet clear. Here we demonstrate the implication of oxidative stress in the development of mitochondrial dysfunction and insulin resistance in response to NOD2 activation in skeletal muscle cells. Treatment with the selective NOD2 ligand muramyl dipeptide (MDP) increased mitochondrial reactive oxygen species (ROS) generation in L6 myotubes.

Fructose induces mitochondrial dysfunction and triggers apoptosis in skeletal muscle cells by provoking oxidative stress.

Mitochondrial dysfunction in skeletal muscle has been implicated in the development of insulin resistance, a major characteristic of type 2 diabetes. There is evidence that oxidative stress results from the increased production of reactive oxygen species and reactive nitrogen species leads to mitochondrial dysfunction, tissue damage, insulin resistance, and other complications observed in type 2 diabetes. It has been suggested that intake of high fructose contributes to insulin resistance and other metabolic disturbances.

Activation of p38/JNK pathway is responsible for embelin induced apoptosis in lung cancer cells: transitional role of reactive oxygen species.

The natural product embelin has been demonstrated to possess a wide range of therapeutic properties, however, the mechanisms by which it exerts anticancer effects are not yet clear. By monitoring the molecular changes associated during early apoptotic phase, we have identified the crucial role of oxidative stress induced MAP kinase signalling as a predominant mechanism for its anticancer effects. Treatment of A549 lung cancer cells with embelin resulted in the enhancement of phospho-p38 and phospho-JNK levels as early as 4h.