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. Author manuscript; available in PMC: 2011 Sep 1.
Published in final edited form as: Microbes Infect. 2010 May 11;12(10):716–726. doi: 10.1016/j.micinf.2010.04.014

Fig. 3. PKA phosphorylates trans-sialidase recombinant protein in vitro PKAc phosphorylation sites were found to flank ER retention motifs in the members of trans-sialidase superfamily.

Fig. 3

A. In vitro phosphorylation of trans-sialidase recombinant protein by PKA is confirmed.

Lane1, Absence of trans-sialidase recombinant protein as negative control;

Lane 2, Trans-sialidase recombinant protein was phosphorylated in absence of PKI;

Lane 3, PKI inhibited the phosphorylation; − absence of the reagent; + presence of the reagent (for details see MATERIALS AND METHODS).

B. Five trans-sialidase protein sequences interacting with TcPKAc possess RXR (Arg-X-Arg) ER retention motifs in N-terminal. A PKAc phosphorylation site and a PKC phosphorylation site flank with these sites. It has been reported that phosphorylation by PKA and PKC in ER and /or Golgi at these sites suppresses ER retention and regulates surface delivery to membrane. The sequences were lined up at N-terminal position 15, RXR is a typical ER retention signal; RRXT or RXXT (position17–20) is a PKA phosphorylation site and SXR (position 23–25) is a PKC phosphorylation site.

(1). Trans-sialidase Tc00.1047053508563.20;

(2). Trans-sialidase Tc00.1047053509187.10;

(3). Trans-sialidase Tc00.1047053507839.40;

(4). Trans-sialidase Tc00.104753510111.20;

(5). Trans-sialidase Tc00.1047053508285.60.