Galectin-12

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Galectin-12

Galectin-12, a member of the galectin family of animal lectins, is preferentially expressed in adipocytes. We recently reported that this galectin is localized on lipid droplets, specialized organelles for fat storage. Galectin-12 regulates lipid degradation (lipolysis) by modulating lipolytic protein kinase A (PKA) signaling. Mice deficient in galectin-12 exhibit enhanced adipocyte lipolysis, ...

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Galectin-12, an Adipose-expressed Galectin-like Molecule Possessing Apoptosis-inducing Activity.

Galectins constitute a family of proteins that bind to beta-galactoside residues and have diverse physiological functions. Here we report on the identification of a galectin-like molecule, galectin-12, in a human adipose tissue cDNA library. The protein contained two potential carbohydrate-recognition domains with the second carbohydrate-recognition domain being less conserved compared with oth...

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Burn control, an adipocyte-specific function for galectin-12.

F amilies of molecules often have similar functions—think of kinases, transcription factors, chemokines, or Toll-like receptors. The galectins, an evolutionarily ancient family of carbohydrate binding proteins found in organisms from multicellular fungi to humans, are different (1, 2). Galectins are a family of lectins; the family designation is based on highly conserved structural features, pa...

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Galectin-12 in Cellular Differentiation, Apoptosis and Polarization

Galectin-12 is a member of a family of mammalian lectins characterized by their affinity for β-galactosides and consensus amino acid sequences. The protein structure consists of a single polypeptide chain containing two carbohydrate-recognition domains joined by a linker region. Galectin-12 is predominantly expressed in adipose tissue, but is also detected in macrophages and other leukocytes. D...

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Editorial: Feel the burn: blocking galectin-12 helps leukemic cells differentiate while staying lean.

Neoplastic disease continues to represent one of the most formidable challenges in modern medicine. Many neoplastic lesions stem from the cumulative outcome of a variety of genetic mutations, allowing cells to rely on multiple and often redundant pathways to sustain undesirable growth [1]. In contrast, several forms of leukemia appear to result from unique translocation events that lead to the ...

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ژورنال

عنوان ژورنال: Adipocyte

سال: 2012

ISSN: 2162-3945,2162-397X

DOI: 10.4161/adip.19465