insulin receptor

They scored a hit on the human gene that makes the insulin receptor.

There were also no changes in the phosphorylation of the insulin receptors.

The insulin receptor is a protein embedded in the outer wall of human cells.

It is taken into cells through an insulin receptor that sits on cell membranes.

Another example is the binding of insulin to insulin receptors.

This process is illustrated by the insulin receptor sites on target cells in a person with type 2 diabetes.

Affected individuals have an insulin receptor with greatly impaired functionality.

Gestational diabetes is caused when the insulin receptors do not function properly.

One of the identified targets of miR-144 is insulin receptor substrate 1.

Quantitation of the class I disulfides of the insulin receptor.

The interference probably occurs at the level of the cell signaling pathway behind the insulin receptor.

Insulin enters cells by first binding to target insulin receptors.

There are a large number of TK enzymes in the body, including the insulin receptor.

It was seen to produce an insulin-like effect by acting on cellular signals downstream of the insulin receptor.

Type two is the most common and is caused by deficiency or inadequacy of insulin receptors in cells.

The insulin receptor system, in contrast, appears to diminish the efficacy of endosomal signaling.

There is a 60% homology between IGF-1R and the insulin receptor.

This in turn promotes insulin receptor activity, thus eliciting improved insulin sensitivity.

It interacts with the insulin receptor, and has been confused with glucose tolerance factor.

This autosomal recessive disorder results in a totally non-functional insulin receptor.

Gonadotropes have insulin receptors, which can be overstimulated by too high insulin levels.

Ectonucleotide pyrophosphatase/phosphodiesterase 1 has been shown to interact with Insulin receptor.

Proliferation of HL-60 cells occurs through the transferrin and insulin receptors, which are expressed on cell surface.

The cause of the disease is the lack of a fully functional insulin receptor, which has a profound effect during fetal development and thereafter.

But it is possible that its overexpression impairs the ability of the insulin receptor to activate cellular enzymes.