From our data, we postulate that defects in cilia of the photoreceptor cells lead to apoptosis, hypothetically releasing peptides and cell debris that activate microglial cells.
Based on our data, we postulate that STIM1 is the major SOCE signal transmitter in neurons, whereas STIM2 has primary responsibility for equilibrium calcium homeostasis.
Based on our data, we postulate novel linkages between the Igf-1 level, aging, and the stem cell compartment.
Given our data, we postulate that therapies targeting IL-17 production, and perhaps IL-10R expression, would prove effective in treatment of SLE-accelerated atherosclerosis.
Based on previous results and our data we postulate that mammary lipid synthesis cannot rely solely on transcriptional regulation via SREBP1 which is probably inhibited or controlled by INSIG1.
The current study demonstrates that in cisplatin-treated cells silencing TBX2 disrupts the ATM-CHK2-p53 axis, and based on our data we postulate that TBX2 is required for activating CHK2, which phosphorylates p53 leading to its stabilisation and its ability to activate downstream targets.
Given the variety of efference copy signals present in parietal cortex (Andersen, 1997) and the correlation observed between the REH (pursuit in darkness) and REW (pure simulated rotation) responses in our data, we postulate that VIP contains an integrated representation of rotation that relies on both visual signals and efference copy inputs.
These data postulate that, although the overall sequence conservation is around 60% of identity, pullulanase enzymatic activity well correlates between SAP and PulA.
Based on our data, PhaZ2 is postulated to affect granule density.
In part, our data supports the hypothesis postulated by Rittweger et al. (2006) that the large number of contraction relaxation cycles during resistive vibration exercise (Blottner et al. 2006) may be effective in preserving muscle fibre contractile properties.
