Target type: biologicalprocess
The chemical reactions and pathways involving heme, any compound of iron complexed in a porphyrin (tetrapyrrole) ring. [GOC:jl, ISBN:0124325653]
Heme metabolic process is a complex and essential biological pathway that involves the synthesis, transport, and degradation of heme. Heme is a porphyrin ring complex containing a ferrous ion, which plays a crucial role in various biological functions, most notably as the prosthetic group of hemoglobin, myoglobin, and cytochromes. The process begins with the synthesis of porphyrins, which are tetrapyrrole macrocycles. Porphyrin biosynthesis occurs primarily in the mitochondria and cytoplasm of erythroid cells, but also in other cell types. The pathway starts with the condensation of succinyl CoA, derived from the citric acid cycle, and the amino acid glycine. This reaction yields α-amino-β-ketoadipate, which is subsequently decarboxylated to δ-aminolevulinate. Two molecules of δ-aminolevulinate then condense to form porphobilinogen, a monopyrrole derivative. Four molecules of porphobilinogen undergo a series of complex enzymatic reactions to form protoporphyrin IX, the immediate precursor of heme. The iron atom is incorporated into protoporphyrin IX by the enzyme ferrochelatase, resulting in the formation of heme. Heme synthesis is tightly regulated by the availability of substrates and the activity of key enzymes. Once synthesized, heme is transported to various cellular compartments, including mitochondria, where it serves as a prosthetic group for various enzymes. The degradation of heme occurs primarily in the spleen, where senescent red blood cells are broken down. The heme molecule is cleaved by the enzyme heme oxygenase, which releases iron and biliverdin, a green pigment. Biliverdin is then reduced to bilirubin, a yellow pigment, which is transported to the liver and conjugated with glucuronic acid. The conjugated bilirubin is excreted into the bile and ultimately eliminated in the feces. The heme metabolic process is essential for maintaining normal oxygen transport, cellular respiration, and other vital biological functions. Disruptions in this pathway can lead to various disorders, including porphyrias, which are characterized by defects in heme biosynthesis, and iron-deficiency anemia, which can result from impaired heme synthesis or increased heme degradation.'
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Protein | Definition | Taxonomy |
---|---|---|
Proton-coupled folate transporter | A proton-coupled folate transporter that is encoded in the genome of human. [PRO:DNx, UniProtKB:Q96NT5] | Homo sapiens (human) |
Proton-coupled folate transporter | A proton-coupled folate transporter that is encoded in the genome of human. [PRO:DNx, UniProtKB:Q96NT5] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
methotrexate | dicarboxylic acid; monocarboxylic acid amide; pteridines | abortifacient; antimetabolite; antineoplastic agent; antirheumatic drug; dermatologic drug; DNA synthesis inhibitor; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; immunosuppressive agent | |
10-propargyl-10-deazaaminopterin | 10-propargyl-10-deazaaminopterin: structure in first source pralatrexate : A pteridine that is the N-4-[1-(2,4-diaminopteridin-6-yl)pent-4-yn-2-yl]benzoyl derivative of L-glutamic acid. Used for treatment of Peripheral T-Cell Lymphoma, an aggressive form of non-Hodgkins lymphoma. | N-acyl-L-glutamic acid; pteridines; terminal acetylenic compound | antimetabolite; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor |
raltitrexed | N-acyl-amino acid | ||
pemetrexed | pemetrexed disodium : An organic sodium salt that is the disodium salt of N-{4-[2-(2-amino-4-oxo-4,7-dihydro-1H-pyrrolo[2,3-d]pyrimidin-5-yl)ethyl]benzoyl}-L-glutamic acid. Inhibits thymidylate synthase (TS), 421 dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT). | N-acyl-L-glutamic acid; pyrrolopyrimidine | antimetabolite; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; EC 2.1.1.45 (thymidylate synthase) inhibitor; EC 2.1.2.2 (phosphoribosylglycinamide formyltransferase) inhibitor |