Disease relevance of Slc16a3

• Only the MCT4 promoter was activated (>2-fold) by hypoxia [1].

High impact information on Slc16a3

• These were just upstream from the transcription start site and also found in the mouse MCT4 promoter [1].
• MCT3, which is expressed in the basolateral membrane of the RPE wild-type mouse, was expressed at very low levels in both the apical and basolateral membranes of the Bsg(-/-) mouse [2].
• We examined whether the quantity of exercise performed influences the expression of monocarboxylate transporter (MCT) 1 and MCT4 in mouse skeletal muscles (plantaris, tibialis anterior, soleus) and heart [3].
• MCT4 mRNA was not detected in human oocytes and embryos, but was present in mouse oocytes and embryos [4].

Chemical compound and disease context of Slc16a3

• The plasma membrane lactate transporter MCT4, but not MCT1, is up-regulated by hypoxia through a HIF-1alpha-dependent mechanism [1].

Other interactions of Slc16a3

• These studies have shown that mild exercise training fails to increase MCT4 and that changes in MCT1 are complex, depending not only the accumulated exercise but also on the stage of training [3].

Analytical, diagnostic and therapeutic context of Slc16a3

• To clarify the role of MCT in development, transport characteristics for DL-lactate were examined, as were mRNA expression and protein localisation for MCT1 and MCT3, using confocal laser scanning immunofluorescence in freshly collected and cultured embryos [5].

References