Lecture 48

Question 1

_____ must be synthesized from Uracil in cells undergoing DNA synth/replication.

Answer 1

THYMINE

Question 2

Nucleotide _____ phosphate kinase converts Nucleotide ______phosphates to diphosphates, whereas Nucleotide _____phosphate kinases convert the diphosphates to triphosphates.

Answer 2

Nucleotide MONOphosphate kinases convert nucleotide MONOphosphates to diphosphates and Nucleotide DIphosphate kinases convert di to tri.

Question 3

Nucleotide monophosphate kinases typically recognize the ____ of nucleotides, whereas diphosphate kinases recognize the _____.

Answer 3

Monophosphate kinases typically recognize the BASE, whereas diphosphate kinases recognize the PHOSPHATE.

Question 4

_____ linkage between ribose and the base of nucleosides/tides (tides have phosphates) is between the ____ carbon of ribose and _____ position N in the base.

Answer 4

GLYCOSIDIC linkage between ribose and base of nucleosides/tides is between the 1 carbon of the ribose and the 9 position N of the base.

Question 5

The ribose component of nucleosides/tides comes from the ____ ____ ____ (PPP.) ____-6-P is converted to 6-phosphogluconolactone via the enzyme ____-6-P _____ (which requires _____ as a cofactor), and in two more steps the ribose-5-P is formed.

Answer 5

From the PENTOSE PHOSPHATE PATHWAY. G-6-P is converted to 6-Phosphogluconolactone via the enzyme G-6-P DEHYDROGENASE (which requires NADP as a cofactor), and in two more steps the ribose-5-P is formed.

Question 6

The biosynthesis of Purines begins with synthesis of ______.

Answer 6

RIBOSE-5-P

Question 7

One of the rate limiting steps in purine synthesis involves the conversion of R-5-P to ______ via the enzyme Ribose Phosphate pyrophospho-kinase and ATP. This step can be feedback inhibited by ___, ___, and ____.

Answer 7

Conversion of R-5-P to PRPP. This step can be feedback inhibited by IMP, AMP, and GMP.

Question 8

The major regulatory step in Purine biosynth involves the conversion of PRPP to 5-_________ via the enzyme Amidophosphoribosyl transferase, using ______ (converted to ______ )as an amino source.

Answer 8

Conversion of PRPP to 5-PHOSPHORIBOSYLAMINE via the enzyme Amidophosphoribosyl transferase, using GLUTAMINE (converted to GLUTAMATE) as an amino source.

Question 9

Amidophosphoribosyl transferase is feedback inhibited by ____, ____, and ____ (the monophosphate versions of the particular purines that are made in the reaction.)

Answer 9

AMP, IMP, and GMP.

Question 10

The AAs involved in purine biosynth are: 2 _____, one _____, and one Apartate, with 2 C units contributed by _____ (single C unit carrier.)

Answer 10

AAs involved in Purine biosynth are: 2 GLUTAMINES, one GLYCINE, and one ASPARTATE, with 2 C units contributed by THF.

Question 11

____ is the nucleotide precursor for both AMP and GMP, with _____ as its base.

Answer 11

IMP is the precursor with HYPOXANTHINE as its base.

Question 12

____ acid is added to IMP to form Adenylosuccinate. This process requires _____. Adenylosuccinate loses _____ to form AMP.

Answer 12

ASPARTIC Acid is added to IMP to for Adenylosuccinate. This process requires GTP. Adenylosuccinate loses FUMARATE to form AMP.

Question 13

To form GMP, an amino group is transferred from _____ (leaving _____) onto IMP. This process requires ____.

Answer 13

An amino group is transferred from GLUTAMINE (leaving GLUTAMATE) onto IMP. This process requires ATP.

Question 14

______ Acid is a drug used to prevent graft rejection. It acts as a ______ uncompetitive inhibitor of IMP dehydrogenase.

Answer 14

MYCOPHENOLIC acid is a drug used to prevent graft rejection. It acts as a REVERSIBLE uncompetitive inhibitor of IMP DH.

Question 15

____ acid is the final degradation product for Purines.

Answer 15

URIC

Question 16

The phosphate of Nucleotide monophosphates can be removed via the enzyme ______, and the ribose can be removed via the enzyme ______, reducing the nucleoside monophosphates to _____bases and finally uric acid.

Answer 16

the phosphate can be removed via NUCLEOTIDASES, and the ribose can be removed via PHOSPHORYLASES.

Question 17

Nucleobases can be “salvaged” back to Nucleotidemonophosphates via addition of ______ (which loses a pyrophosphate) by the enzyme ________ transferase.

Answer 17

via addition of PRPP (which loses a pyrophosphate) by the enzyme PHOSPHORIBOSYL tarnsferase.

Question 18

Phosphorylase cleaves the _____ bond of Nucleotides while Nucleotidase cleaves the Carbon-____ bond.

Answer 18

Phosphorylase cleaves the GLYCOSIDIC bond while Nucleotidase cleaves the Carbon-PHOSPHATE bond.

Question 19

AMP and Adenosine lose ____ in the degradation pathway via ______ enzymes. This is a source of free _____.

Answer 19

They lose NH4+ via DEAMINASE enzymes. This is a source of free NH4+.

Question 20

Gout is caused by defects in the _____ pathway, speifically in ____ synthase and HGPRT, that causes _____, and eventually Uric acid, to build up. This leads to a net increase in the _____ and _____ pathways.

Answer 20

Caused by defects in the SALVAGE pathway, specifically in PRPP synthase and HGPRT,
causing PRPP, and eventually uric acid, to build up. This leads to a net increase in the BIOSYNTHETIC and DEGRADATION pathways.

Question 21

Allopurinol acts as a ____ inhibitor of _____ oxidase, so less Uric acid is produced from _____. There is also a decrease in _____.

Answer 21

It acts as a COMPETITIVE inhibitor of XANTHINE oxidase, so less URIC acid is produced from XANTHINE. There is also a decrease in PRPP.

Question 22

SCID is caused by ____ recessive mutation in Adenine _____, which causes a toxic buildup of ____. As a result, both _____ and _____ cells are reduced.

Answer 22

It is caused by an AUTOSOMAL recessive mutation in Adenine DEAMINASE (ADA), which causes a toxic buildup of dAMP. As a result, both T and B cells are reduced.

Question 23

____ ___ syndrome is characterized by a(n) ______ recessive mutation leading to a complete lack of _____. These patients tend to self-inflict harm (i.e. biting lips.)

Answer 23

Lesh Nyhan syndrom is characterized by an AUTOSOMAL recessive mutation leading to a complete lack of HGPRT.