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They do this by "hijacking" the proteins within the membrane. Whilst there has been extensive research into how bacteria bind our cells, no universal mechanisms (used by all bacteria) are known. Different bacterial species have been shown to hijack different proteins, which causes problems with therapeutic design. I have discovered that a family of human cell membrane proteins, the tetraspanins, are extremely important in the binding of multiple bacterial species to our cells. Targeting tetraspanins using drugs reduces bacterial binding to multiple types of human cells by greater than 50%. The tetraspanins form part of our cell membranes and act as "organisers", bringing together lots of other proteins to form large protein "islands" in the cell membrane. Bacteria do not directly attach to the tetraspanins but I hypothesise that the tetraspanins organize the proteins required for bacterial binding and it is therefore the loss of this organization which results in reduced bacterial adhesion to our cells when the tetraspanins are blocked.
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The ocular surface (2023): 211-218
bioRxivpp.1-49, (2020)
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