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Decrease in Membrane Phospholipid Unsaturation Induces Unfolded Protein Response*
TLDR
It is shown that stearoyl-CoA desaturase 1 (SCD1) knockdown increased the amount of saturated fatty acids and decreased that of monounsaturated fatty acids in phospholipids without affecting the amount or the composition of free fatty acid and induced unfolded protein response (UPR).
Targets of TGF-β Signaling in Caenorhabditis elegans Dauer Formation
TLDR
This work genetically characterized and cloned a putative transducer of DAF-7 signaling called daf-14 and found that it encodes a Smad protein, a highly unusual structure completely lacking the N-terminal domain found in all other Smad proteins known to date.
Morphologically defined sub-stages of C. elegans vulval development in the fourth larval stage
TLDR
This scheme allows the developmental timing of an L4 individual to be determined at approximately one-hour resolution without the need to resort to time course experiments and will enable more precise description of gene expression and other developmental events.
Intracellular phosphatidylserine is essential for retrograde membrane traffic through endosomes
TLDR
It is reported that PS is essential for retrograde membrane traffic at recycling endosomes (REs) and a unique PH domain is identified that specifically recognizes PS but not polyphosphoinositides.
LPIAT1 regulates arachidonic acid content in phosphatidylinositol and is required for cortical lamination in mice
TLDR
Studies using knockout mice of lysophosphatidylinositol acyltransferase 1 reveal that AA-containing PI plays a crucial role in cortical lamination and neuronal migration during brain development.
Study of LiFePO4 by Cyclic Voltammetry
A systematic study of LiFePO 4 with cyclic voltammetry (CV) was conducted using thin electrodes with a loading of 4 mg/cm 2 . Peak current of the CV profile was proportional to the square root of
The C. elegans ROR receptor tyrosine kinase, CAM-1, non-autonomously inhibits the Wnt pathway
TLDR
It is found that loss and overexpression of cam-1 causes reciprocal defects in Wnt-mediated cell-fate specification, and the molecular and genetic analyses revealed that the CAM-1 extracellular domain (ECD) is sufficient to non-autonomously antagonize multiple Wnts, suggesting that the Cam-1/ROR ECD sequesters WNTs.
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