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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Vesicles incorporate different coat protein subunits in different cell locations, which changes the properties of the coat, such as the shape and geometry of the transport vesicles. Thus, vesicle coat proteins also play a significant role in cargo selection.
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Binding sites linkages can regulate a protein's function.  For example, enzyme activity is often regulated through a feedback mechanism where the end product of the biochemical process serves as an inhibitor.
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Quantitative Measurement of γ-Secretase-mediated Amyloid Precursor Protein and Notch Cleavage in Cell-based Luciferase Reporter Assay Platforms
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BACE1: More than just a β-secretase.

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Beta-site amyloid precursor protein cleaving enzyme-1 (BACE1) is implicated in metabolic diseases beyond Alzheimer's. BACE1 inhibitors show promise for treating obesity and related conditions.

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Area of Science:

  • Metabolic disease research
  • Enzyme function and regulation
  • Biochemistry of metabolic disorders

Background:

  • Beta-site amyloid precursor protein cleaving enzyme-1 (BACE1) is primarily known for its role in Alzheimer's disease pathogenesis.
  • BACE1 is expressed in various cell types beyond the brain, including pancreatic, adipose, liver, and vascular cells.
  • Pathological BACE1 overexpression in these peripheral tissues is linked to metabolic diseases like type 2 diabetes, obesity, and cardiovascular disease.

Purpose of the Study:

  • To review the regulation and dysregulation of BACE1 in disease.
  • To elucidate the role of BACE1 in metabolic regulation through substrate cleavage.
  • To explore the therapeutic potential of BACE1 inhibitors for obesity and its comorbidities.

Main Methods:

  • Review of existing literature on BACE1 function, regulation, and involvement in metabolic diseases.
  • Analysis of data from BACE1 knockout mouse models.
  • Examination of clinical trial data for BACE1 inhibitors in metabolic contexts.

Main Results:

  • BACE1 knockout mice exhibit phenotypes suggestive of a physiological role in energy metabolism, including reduced weight gain and increased energy expenditure.
  • BACE1 inhibition in clinical trials has led to observed weight loss.
  • BACE1 regulates metabolism through the cleavage of various substrates.

Conclusions:

  • BACE1 plays a significant role in regulating energy metabolism and homeostasis.
  • BACE1 inhibitors represent a potential novel therapeutic strategy for obesity and associated metabolic disorders.