Protein tyrosine phosphatase 1B (PTP1B) is considered as a major negative regulator of insulin receptor (IR) signaling. IR signaling in retina has been demonstrated to be neuroprotective. Photoreceptor-specific deletion of PTP1B results in enhanced retinal IR-mediated neuroprotection indicating the importance of PTP1B as a negative regulator in the retina. Elevated levels of retinal PTP1B activity have been observed in mice lacking retinal pigment epithelium (Rpe65 -/-), a mouse model of leber congenital amaurosis (LCA-type 2), retinitis pigmentosa and diabetic retinopathy animal models. This enhanced PTP1B activity could downregulate the IR signaling which may contribute to the death of photoreceptor neurons and ultimately lead to retinal degenerations. The potential therapeutic agents that specifically reduce or inhibit the PTP1B activity could be beneficial in protecting or delaying the photoreceptor cell death in the retinal degenerative diseases.
|Name||Advances in experimental medicine and biology|
|Conference||International Symposium on Retinal Degenerations (14th : 2010)|
|Period||13/07/10 → 17/07/10|
- Insulin Receptor
- Protein Tyrosine Phosphatase-1B
- Retinal Degeneration