shankar jan
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Could someone please help me understand this or reword it in a way to help me understand?
The fusion stuff is confusing me a bit.
Also, am not sure what "the receptor portions of these hybrid fusion proteins are dragged together by the dimerising proteins to which they have become joined" means.

Any help will be very much appreciated!!
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shankar jan
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Jpw1097
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(Original post by shankar jan)
Could someone please help me understand this or reword it in a way to help me understand?
The fusion stuff is confusing me a bit.
Also, am not sure what "the receptor portions of these hybrid fusion proteins are dragged together by the dimerising proteins to which they have become joined" means.

Any help will be very much appreciated!!
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This is the way some receptors work - specifically receptor tyrosine kinases. When a growth factor binds to the receptor, the receptor dimerises (i.e. joins together) with another receptor. The tyrosine kinase domains then phosphorylate each other. This then activates a signalling cascade that leads to cell proliferation, etc.

Now, suppose you have a mutation in the gene that codes for this receptor, such that it now dimerises and activates the signalling cascade in the absence of the growth - that is, it is constitutively active - it will now cause cell proliferation even in the absence of growth factor. This is one of the mechanisms involved in tumourigenesis.
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shankar jan
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(Original post by Jpw1097)
This is the way some receptors work - specifically receptor tyrosine kinases. When a growth factor binds to the receptor, the receptor dimerises (i.e. joins together) with another receptor. The tyrosine kinase domains then phosphorylate each other. This then activates a signalling cascade that leads to cell proliferation, etc.

Now, suppose you have a mutation in the gene that codes for this receptor, such that it now dimerises and activates the signalling cascade in the absence of the growth - that is, it is constitutively active - it will now cause cell proliferation even in the absence of growth factor. This is one of the mechanisms involved in tumourigenesis.
Thanks so much I get this - not sure why I was confused about it earlier on. You explained it quite perfectly - apologies for my ignorance.
I think I've hopefully got it now
I think receptor dimerisation doesn't always happen because of gene fusion ( for example kinase-linked receptors dimerise and it's not because of gene fusion - but then I wonder how kinase-liked receptors form?..) -->this is the one thing I am confused about at the moment

The top part of a hybrid fusion protein is the receptor (from the surface of the cell upwards) and the bottom part of the hybrid fusion protein is a protein which dimerises when activated. In a normal cell, when a growth factor binds to the receptor..it gets activated and then dimerises. In a malignant cell, when a growth factor is attached to the receptor part of the hybrid fusion protein, then the receptor is activated and then dimerises - this is because the bottom part of the hybrid fusion protein is stimulated and therefore drags the 2 proteins together, resulting in the receptor parts of the proteins also dimerising.. so same process as in a normal cell.
However, in malignant cell, the receptor is constantly active and will keep on stimulating cell proliferation even in the absence of growth factors like you kindly mentioned.

But to be honest, I feel like to say that a receptor dimerises is a bit wrong, especially in the case of a hybrid fusion protein because only the top bit is a receptor. Dimerisation is not only joining together but also the formation of bonds between two things. When the bottom parts of the 2 hybrid proteins dimerise, then this also leads to the top parts (the receptors) touching each other but that doesn't necessarily mean that the 2 receptors dimerise.

Would really love to hear your thoughts, although you have helped me so much! No worries at all if you're busy
Last edited by shankar jan; 2 years ago
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