V.R.T.
Senior Member (Voting Rights)
Good to hear! Is the timeframe for the HLA analysis similar?Almost certainly this year, hopefully within the next 6 months.
Good to hear! Is the timeframe for the HLA analysis similar?Almost certainly this year, hopefully within the next 6 months.
Yes.Good to hear! Is the timeframe for the HLA analysis similar?
So MCTS1 seems to sometimes work in concert with E2F1.
Somewhere in all this is a causal reality. I think we might find it but don't ask me where at the moment.
Whereas I am standing on the cliff up above yelling 'maybe look over there! Or over there!' to nobody in particular whilst gesticulating wildly at various stretches of beach.My general approach is like someone flailing around on a beach picking up pebbles and holding them up to passers-by and saying, in a hopeful tone, ‘is this interesting?’
*looks up to the cliff, tries to follow where @V.R.T. Is pointing, runs over and picks up another pebble* “this one?”Whereas I am standing on the cliff up above yelling 'maybe look over there! Or over there!' to nobody in particular whilst gesticulating wildly at various stretches of beach.
Can only speak to what we know other people are doing. I have circulating proteomics on 100 people being done as a small part of one of my studies but it is using olink, not somascanI was going to ask those more knowledgeable and experienced in this field (like @DMissa ) what the chances are of someone else looking at ME/CFS proteomics would be of reproducing this.
Failure to efficiently clear apoptotic cells (efferocytosis) is associated with autoimmunity. Complement component C1q is required for efferocytosis, and deficiency in C1q leads to development of autoimmunity. We recently identified a novel molecular mechanism for C1q-dependent efferocytosis in mouse macrophages. We found that C1q elicited the expression and function of Mer tyrosine kinase and the Mer ligand, Ga6: a receptor-ligand pair that mediates efferocytosis. To define the signal transduction pathway downstream of C1q, pathway analysis was performed using the transcriptome from C1q-treated macrophages. This analysis revealed that the adiponectin signaling pathway was significantly upregulated with C1q. Adiponectin is a well characterized adipokine with critical roles in glucose and fatty acid metabolism, and it is structurally homologous to C1q. Similar to C1q, adiponectin triggered expression of Mer that correlated with enhanced engulfment of apoptotic cells, and a soluble Mer-Fc fusion protein inhibited adiponectin-dependent efferocytosis.