Biotin

Holocarboxylase synthetase synergizes with methyl CpG binding protein 2 and DNA methyltransferase 1 in the transcriptional repression of long-terminal repeats

“…2 The classical role of HLCS is to catalyze the covalent binding of biotin to five distinct carboxylases in cytoplasm and mitochondria. 3 More recently, it became evident that HLCS also enters the cell nucleus 4,5 where it binds to chromatin in a punctuate, locus-specific pattern. 6,7 Unambiguous evidence suggests that recombinant HLCS catalyzes biotinylation of histone H3 in vitro and that HLCS knockdown causes a loss in histone H3 and H4 biotinylation marks in vivo.…”

Influences of dietary biotin and avidin on growth, survival, deficiency syndrome and hepatic gene expression of juvenile Nile tilapia Oreochromis niloticus

“…One likely mechanism leading to increased body lipid in fish fed higher avidin-supplemented diet is that diminished activities of biotindependent carboxylases cause abnormal metabolism of fatty acids in severe biotin deficiency condition. It is evident that particularly acetyl-CoA carboxylase plays a role in fatty acid synthesis in mammals and other animals (Zempleni 2001). Consistent with this hypothesis, acetyl-CoA carboxylase was reduced in biotindeficient chicks, but activities of fatty acid synthetase and both the mitochondrial and microsomal systems of fatty acid elongation were unaffected (Marson and Donaldson 1972).…”

Biotin

“…Biotinidase catalyzes the release of biotin from breakdown products of carboxylases and, therefore, plays a crucial role in biotin recycling (1). Mutations in the biotinidase gene impair the recycling of biotin and lead to a substantial urinary loss of biotin in form of biotinylated peptides.…”

“…I n mammals, biotin serves as a covalently bound coenzyme for 5 carboxylases: acetyl-CoA carboxylases 1 and 2, propionyl-CoA carboxylase (PCC), 5 3-methylcrotonyl-CoA carboxylase (MCC), and pyruvate carboxylase (1). Acetyl-CoA carboxylase 1 localizes in the cytoplasm, where it catalyzes the binding of bicarbonate to acetyl-CoA in a key step in fatty acid synthesis.…”

“…Biotin status is typically assessed by quantifying the urinary excretion of biotin and its major metabolites (w120 nmoles/d), the activity of PCC or MCC in lymphocytes, and the abundance of biotinylated carboxylases in cell extracts (1). Biotin deficiency causes low activity of MCC, thereby shunting metabolites from leucine metabolism to alternative pathways.…”