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It was originally proposed that TNF homotrimers induce signalling by aggregation of TNFRs, although subsequent models proposed a minimal unit of receptor activation involving preformed receptor dimers on the cell surface which are allosterically modified by ligand binding [ 27].
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For example, to date, there have been several influential models proposing a dorsal-ventral axis across the lateral portion of the prefrontal cortex.
Other models propose a continuous and iterative lobe initiation process during cell morphogenesis [ 20, 27].
Current models propose a role for TelRNA/TERRA in controlling telomerase activity.
Interval models propose a way of representing the duration of an interval via a resettable accumulator-counter mechanism.
This hypothesis is based on models proposing a prominent role of gene conversion and DNA repair in intron loss [ 84, 85].
Both models propose a duality of conversion rate limitations where neither cell mass nor substrate concentration can be assumed in excess.
In the 1980s, a climate model proposed a thick atmosphere of heat-trapping carbon dioxide, raising the average surface temperature to 185 degrees Fahrenheit, not quite boiling.
The model proposed a transition between an open state, to which ATP binds, and a closed ATP-bound state.
A complementary study performed on the same model proposed a concurrent role for Transforming Growth Factor-β (TGF-β) and TNF-α in promoting splenocyte apoptosis [ 123].
An alternative model proposed a direct recognition of misfolded proteins by Ire1 (Credle et al., 2005; Gardner and Walter, 2011; Promlek et al., 2011).
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