Expression Profiles of Mouse Kell, XK, and XPLAC mRNA
Soohee Lee 1*, Quan Sha 1, Xu Wu 1, Giulia Calenda 1 and Jianbin Peng 1
1 New York Blood Center, New York, New York
* To whom correspondence should be addressed. E-mail: solee{at}nybloodcenter.org.
Submitted on October 23, 2006
Accepted on 7 December 2006
 |
Abstract |
|---|
Kell and XK are related since, in red cells, they exist as a disulfide bonded complex. Kell is an endothelin-3-converting enzyme and XK is predicted to be a transporter. Absence of XK, which is accompanied by reduced Kell on red cells, results in acanthocytosis and late onset forms of central nervous system and neuromuscular abnormalities that characterize the McLeod syndrome. In this study the expression of mouse XK, XPLAC, a homolog of XK, and of Kell were compared by in situ hybridization histochemistry (ISHH) and RT-PCR. ISHH showed that Kell and XK are co-expressed in erythroid tissues. ISHH detected XK, but not Kell, mRNA in testis but RT-PCR indicated that both Kell and XK are co-expressed. XK, but not Kell, was significantly expressed in brain, spinal cord, small intestine, heart, stomach, bladder and kidney. ISHH did not detect XK in skeletal muscle but RT-PCR did. In brain, XK was predominantly expressed in neuronal rather than in supportive cells. By contrast, XPLAC was predominantly expressed in the thymus. The co-expression of Kell and XK in erythroid tissues and the different expressions in non-erythroid tissues suggest that XK may have a complementary hematological function with Kell and a separate role in other tissues.
Key Words:
in situ hybridization histochemistry, RT-PCR, McLeod syndrome, mouse tissue expression
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati 
Twitter What's this?
