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Passage Nerve Cells Must Maintain the Composition of Their Myelin Sheaths

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Passage
Nerve cells must maintain the composition of their myelin sheaths to function properly.  Galactocerebroside (GC) , shown in Figure 1, is a hydrolyzable lipid and an important component of the myelin sheath.
Passage Nerve cells must maintain the composition of their myelin sheaths to function properly.  Galactocerebroside (GC) , shown in Figure 1, is a hydrolyzable lipid and an important component of the myelin sheath.    <strong>Figure 1</strong>  Structure of the myelin sheath component galactocerebrosideHomeostasis of GC is maintained by its dynamic synthesis and degradation, as shown in Figure 2.  GC is synthesized by the enzyme ceramide galactosyltransferase (CGT)  using UDP-galactose (UDP-Gal)  and ceramide (Cer)  as substrates.  It is degraded by the enzyme galactocerebrosidase (GalC) , which hydrolyzes the glycosidic bond to release galactose (Gal)  and ceramide.  A deficiency in GalC activity leads to a buildup of GC, and prior research has connected this buildup with neurodegeneration.    <strong>Figure 2</strong>  Schematic of GCT and GalC activity in healthy and GalC deficient cellsOver 100 inactivating GalC mutations have been identified.  Five of the most common mutations are listed in Table 1.  The changes to both DNA and amino acid sequence are shown.<strong>Table 1</strong>  Five Common Galactocerebrosidase Mutations    -Based on Table 1, the D187V form of GalC resulted from what type of nucleotide change? A) A pyrimidine was replaced by a different pyrimidine B) A pyrimidine was replaced by a purine C) A purine was replaced by a pyrimidine D) A purine was replaced by a different purine Figure 1  Structure of the myelin sheath component galactocerebrosideHomeostasis of GC is maintained by its dynamic synthesis and degradation, as shown in Figure 2.  GC is synthesized by the enzyme ceramide galactosyltransferase (CGT) using UDP-galactose (UDP-Gal) and ceramide (Cer) as substrates.  It is degraded by the enzyme galactocerebrosidase (GalC) , which hydrolyzes the glycosidic bond to release galactose (Gal) and ceramide.  A deficiency in GalC activity leads to a buildup of GC, and prior research has connected this buildup with neurodegeneration.
Passage Nerve cells must maintain the composition of their myelin sheaths to function properly.  Galactocerebroside (GC) , shown in Figure 1, is a hydrolyzable lipid and an important component of the myelin sheath.    <strong>Figure 1</strong>  Structure of the myelin sheath component galactocerebrosideHomeostasis of GC is maintained by its dynamic synthesis and degradation, as shown in Figure 2.  GC is synthesized by the enzyme ceramide galactosyltransferase (CGT)  using UDP-galactose (UDP-Gal)  and ceramide (Cer)  as substrates.  It is degraded by the enzyme galactocerebrosidase (GalC) , which hydrolyzes the glycosidic bond to release galactose (Gal)  and ceramide.  A deficiency in GalC activity leads to a buildup of GC, and prior research has connected this buildup with neurodegeneration.    <strong>Figure 2</strong>  Schematic of GCT and GalC activity in healthy and GalC deficient cellsOver 100 inactivating GalC mutations have been identified.  Five of the most common mutations are listed in Table 1.  The changes to both DNA and amino acid sequence are shown.<strong>Table 1</strong>  Five Common Galactocerebrosidase Mutations    -Based on Table 1, the D187V form of GalC resulted from what type of nucleotide change? A) A pyrimidine was replaced by a different pyrimidine B) A pyrimidine was replaced by a purine C) A purine was replaced by a pyrimidine D) A purine was replaced by a different purine Figure 2  Schematic of GCT and GalC activity in healthy and GalC deficient cellsOver 100 inactivating GalC mutations have been identified.  Five of the most common mutations are listed in Table 1.  The changes to both DNA and amino acid sequence are shown.Table 1  Five Common Galactocerebrosidase Mutations
Passage Nerve cells must maintain the composition of their myelin sheaths to function properly.  Galactocerebroside (GC) , shown in Figure 1, is a hydrolyzable lipid and an important component of the myelin sheath.    <strong>Figure 1</strong>  Structure of the myelin sheath component galactocerebrosideHomeostasis of GC is maintained by its dynamic synthesis and degradation, as shown in Figure 2.  GC is synthesized by the enzyme ceramide galactosyltransferase (CGT)  using UDP-galactose (UDP-Gal)  and ceramide (Cer)  as substrates.  It is degraded by the enzyme galactocerebrosidase (GalC) , which hydrolyzes the glycosidic bond to release galactose (Gal)  and ceramide.  A deficiency in GalC activity leads to a buildup of GC, and prior research has connected this buildup with neurodegeneration.    <strong>Figure 2</strong>  Schematic of GCT and GalC activity in healthy and GalC deficient cellsOver 100 inactivating GalC mutations have been identified.  Five of the most common mutations are listed in Table 1.  The changes to both DNA and amino acid sequence are shown.<strong>Table 1</strong>  Five Common Galactocerebrosidase Mutations    -Based on Table 1, the D187V form of GalC resulted from what type of nucleotide change? A) A pyrimidine was replaced by a different pyrimidine B) A pyrimidine was replaced by a purine C) A purine was replaced by a pyrimidine D) A purine was replaced by a different purine
-Based on Table 1, the D187V form of GalC resulted from what type of nucleotide change?


A) A pyrimidine was replaced by a different pyrimidine
B) A pyrimidine was replaced by a purine
C) A purine was replaced by a pyrimidine
D) A purine was replaced by a different purine

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