Membrane Topology of the C. elegans SEL-12 Presenilin
نویسندگان
چکیده
منابع مشابه
Membrane Topology of the C. elegans SEL-12 Presenilin
Mutant presenilins cause Alzheimer's disease. Presenilins have multiple hydrophobic regions that could theoretically span a membrane, and a knowledge of the membrane topology is crucial for deducing the mechanism of presenilin function. By analyzing the activity of beta-galactosidase hybrid proteins expressed in C. elegans, we show that the C. elegans SEL-12 presenilin has eight transmembrane d...
متن کاملEffects of SEL-12 presenilin on LIN-12 localization and function in Caenorhabditis elegans.
Presenilins have been implicated in the development of Alzheimer's disease and in facilitating LIN-12/Notch activity. Here, we use genetic methods to explore the relationship between C. elegans LIN-12 and SEL-12 presenilin. Reducing sel-12 activity can suppress the effects of elevated lin-12 activity when LIN-12 is activated by missense mutations but not when LIN-12 is activated by removal of t...
متن کاملSEL1L (sel-1 suppressor of lin-12-like (C. elegans))
Hugo: SEL1L Other names: IBD2; SEL1-like Location: 14q24.3-q31 Local order: SEL1L is located within a 'Gene Desert area' or 'Genome Deserts'; centromeric to FLRT2 (fibronectin leucine rich transmembrane protein 2) and telomeric to GTF2A1 (general transcription factor IIA) and TSHRq31 (thyroid stimulating hormone receptor). Note: SEL1L is the human ortholog of the C.Elegans sel-1 (suppressor enh...
متن کاملEvidence for functional and physical association between Caenorhabditis elegans SEL-10, a Cdc4p-related protein, and SEL-12 presenilin.
Mutations in either of two human presenilin genes (PS1 and PS2) cause Alzheimer's disease. Here we describe genetic and physical interactions between Caenorhabditis elegans SEL-10, a member of the Cdc4p family of proteins, and SEL-12, a C. elegans presenilin. We show that loss of sel-10 activity can suppress the egg-laying defective phenotype associated with reducing sel-12 activity, and that S...
متن کاملSuppressors of the egg-laying defective phenotype of sel-12 presenilin mutants implicate the CoREST corepressor complex in LIN-12/Notch signaling in C. elegans.
Presenilin is an essential component of the LIN-12/Notch signaling pathway and also plays a critical role in the genesis of Alzheimer's disease. Previously, a screen for suppressors of the egg-laying defective phenotype caused by partial loss of presenilin activity in Caenorhabditis elegans identified a number of new spr genes that are potentially involved in the regulation of LIN-12/Notch sign...
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ژورنال
عنوان ژورنال: Neuron
سال: 1996
ISSN: 0896-6273
DOI: 10.1016/s0896-6273(00)80231-7