EPHA2

(redirected from CTPA)
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EPHA2

A gene on chromosome 1q36 that encodes a member of the ephrin-A receptor subfamily of receptor tyrosine kinases, which promiscuously bind membrane-bound ephrin-A family ligands residing on adjacent cells, leading to contact-dependent bidirectional signalling into neighbouring cells. Once activated by the ligand ephrin-A1 (EFNA1), it regulates cell adhesion and differentiation through DSG1/desmoglein-1 and inhibition of the ERK1/ERK2 (MAPK3/MAPK1, respectively) signalling pathway. It may participate in UV radiation-induced apoptosis and have a ligand-independent stimulatory effect on chemotactic cell migration.

During development, EPHA2 may function in distinctive aspects of pattern formation and development of several foetal tissues, such as angiogenesis, early hindbrain development and epithelial proliferation, and branching morphogenesis during mammary gland development. It is thought to regulate lens fibre cells’ shape and interactions and to be important for lens transparency development and maintenance. With ephrin-A2 (EFNA2), it may play a role in bone remodelling by regulating osteoclastogenesis and osteoblastogenesis.

EPHA2 interacts with ACP1, ANKS1A, ARHGEF16, CLDN4, DOCK4, ELMO2, INPPL1, PIK3R1, PIK3R2, PIK3R3, PTK2/FAK1, PTPN11, SLA, VAV2, and VAV3. 

Molecular pathology
Defects in EPHA2 cause cataract cortical age-related type 2 (age-related cataract cortical type 2) and cataract posterior polar type 1 (posterior polar cataracts type 2).
References in periodicals archive ?
Patients were divided into two groups, CTPA positive (patients with PE) and CTPA negative (PE excluded), and risk factors were analyzed by calculating medians and percentages, where appropriate.
After initial stabilization, CTPA (Figure-2) was done that showed extensive pulmonary embolism extending from main pulmonary trunk to right and left pulmonary arteries.
An elevated D-dimer, ideally adjusted for age, should prompt evaluation by CTPA.
Only 6 cases underwent directly a CTPA without a conventional chest X-ray first (because of the high clinical suspicion of PE).
5 minutes from the start of IV contrast administration for CTPA.
Both CTPA and VQS are excellent first-line investigations and their availability often determines the first choice.
CTPA is currently the diagnostic modality of choice for the diagnosis of PE.
The primary outcome of this study was the incidence of coagulopathy in patients who had acute PE confirmed by CTPA, and the diagnostic ability of coagulopathy in differentiating between acute PE and other respiratory pathologies in patients who had clinical symptoms and signs suggestive of acute PE requiring CTPA to exclude acute PE.
I tried to calm her by reassuring her that we would never do anything to harm her or her baby, but at the same time privately wondered why a CTPA had been requested at this stage of pregnancy when a Ventilation Perfusion Scan (VQ scan) is generally considered the gold standard in diagnosing PE in pregnant women due to the lower radiation dose and no exposure to intravenous contrast media (Scarsbrook, 2007).
A repeat CTPA was undertaken 2 days later, confirming satisfactory PAA exclusion, with no evidence of residual filling (Figure 5).
The eight-hour orientation session with the additions of the CTPA, the practice course, the extended library online tour, and faculty support with navigating through the online nursing courses revealed increased satisfaction (94.
It can be used as a replacement diagnostic where CTPA is an inappropriate choice based on radiation exposure, renal impairment or contrast allergy.