DPYSL2

(redirected from CRMP2)

DPYSL2

A gene on chromosome 8p22-p21 that encodes a member of the collapsin response mediator protein family, which forms homo- and heterotetramers. DPYSL2 plays a role in neuronal development and polarity, as well as in axon growth and guidance, neuronal growth cone collapse and cell migration.  

Molecular pathology
DPYSL2 has been implicated in multiple neurological disorders; hyperphosphorylation of the encoded protein may play a role in the development of Alzheimer's disease.
Mentioned in ?
References in periodicals archive ?
We determined whether CRMP2 modulates ischemic injury in the retinal of Ocular ischemic syndrome (OIS).
sup][7],[8] CRMP2 is the first member of this family to be discovered and has been studied most frequently.
A number of studies have found that total CRMP2 was decreased due to calpain cleaved in ischemic/hypoxic injury.
The blocked PVDF membrane was incubated with primary rabbit polyclonal antibody against pCRMP2 (T514) (1:1000, Abcam Technology, Cambridge, MA, USA) for 2 h or for 3 h in CRMP2 (1:1000, Cell Signaling Technology, #9393, USA).
To detect the changes of CRMP2 expression and phosphorylation level in the chronic ischemic retina, we used Western blot to evaluate the CRMP2 and p-CRMP2 (Thr514) levels in each group.
Shah, "A derivative of the CRMP2 binding compound lanthionine ketimine provides neuroprotection in a mouse model of cerebral ischemia," Neurochemistry International, vol 61, no.
Dr Calum Sutherland and his team at Dundee University found the protein, called CRMP2, plays an important role in the development of nerve tangles seen in the disease.
He said: "If drugs could be developed that activate this, then they should reverse the abnormal structure of CRMP2 - and hopefully slow down the development of tangles in the brain.
Lipid peroxidation (LP) is involved in triggering postinjury CRMP2 proteolysis.
sup][10] The proteolysis of CRMP2 mediated by calpain following TBI may be a potential inhibitory factor for posttraumatic neurite regeneration.
In this study, we hypothesized that propofol attenuates LP, calpain-induced CRMP2 degradation and programmed cell death, providing neuroprotection during the early period after TBI.
The membrane was then incubated for 3 h at room temperature with a rabbit polyclonal antibody against CRMP2 (Cell Signaling Technology, Danvers, MA, USA) and a mouse monoclonal antibody against aII-spectrin (Merck Millipore, Darmstadt, Germany).