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Ribonucleoside- diphosphate reductase subunit M2 Ribonucleoside- diphosphate reductase subunit M2 B Equilibrative nucleoside transporter 1 Sodium/nucleoside cotransporter 2 Equilibrative nucleoside transporter 2 Adenosine deaminase Deoxyguanosine kinase, mitochondrial Deoxyguanosine kinase, mitochondrial ara-GTP ara-GTP Nelarabine Nelarabine an oxidized thioredoxin dADP H2O ADP reduced thioredoxin H2O ara-Guanosine ATP ara-GMP ADP ATP ara-GDP ADP ATP ADP Na+ Na+ Zinc (II) ion DNA polymerase catalytic subunit DNA ligase 1 DNA primase small subunit Fe2+ DNA synthesis Cytosol Nelarabine is a prodrug, it is converted ara-Guanosine. This last molecule while undergo 3 phosphorylation reactions. T Cell Blood vessel T Cell Apoptosis The apoptosis of the T cells result in the death of the cancerous white blood cells. Due to the inhibition of the DNA synthesis, the inhibition of the DNA polymerase, ligase and primase, and the inhibition of the ribonucleoside reductase, the T cells will go through apoptosis.This drug cause cells to accumulate at the S phase of the cell cycle. Nucleus The incorporation in the DNA results in DNA breaks and the inhibition of DNA synthesis and repair. During the replication of the DNA, this will cause the apoptosis of the T or B cells. The accumulation of ara-GTP inhibits the ribonuclotide reductase. This leads to an imbalance in dNTP. This will impact the DNA synthesis because the dNTP pool will be changed. The imbalanced dNTP pool leads to DNA strand breaks and to the inhibition of the DNA synthesis. Through depletion of the dNTP pool, clofarabine self-potentiates the incorporation of clofarabine triphosphates into DNA. Mitochondrion Probably hrough competitive inhibition, this drug also inhibits the DNA polymerase, the DNA ligase, and the DNA primase.
Nucleus RRM2 RRM2B SLC29A1 SLC28A2 SLC29A2 ADA DGUOK DGUOK ara-GTP ara-GTP Nelarabine Nelarabine an oxidized thioredoxin dADP Water Adenosine diphosphate reduced thioredoxin Water ara-Guanosine Adenosine triphosphate ara-GMP Adenosine diphosphate Adenosine triphosphate ara-GDP Adenosine diphosphate Adenosine triphosphate Adenosine diphosphate Sodium Sodium ORF28 LIG1 PRIM1 DNA synthesis
RRM2 RRM2B SLC29A1 SLC28A2 SLC29A2 ADA DGUOK DGUOK ara-GTP ara-GTP Arranon Arranon AOT dADP H2O ADP RT H2O ara-Gua ATP ara-GMP ADP ATP ara-GDP ADP ATP ADP Na+ Na+ Zinc ORF28 LIG1 PRIM1 Fe2+ DNA syn Cytosol Nelarabine is a prodrug, it is converted ara-Guanosine. This last molecule while undergo 3 phosphorylation reactions. T Cell Blood vessel T Cell Apoptosis The apoptosis of the T cells result in the death of the cancerous white blood cells. Due to the inhibition of the DNA synthesis, the inhibition of the DNA polymerase, ligase and primase, and the inhibition of the ribonucleoside reductase, the T cells will go through apoptosis.This drug cause cells to accumulate at the S phase of the cell cycle. Nucleus The incorporation in the DNA results in DNA breaks and the inhibition of DNA synthesis and repair. During the replication of the DNA, this will cause the apoptosis of the T or B cells. The accumulation of ara-GTP inhibits the ribonuclotide reductase. This leads to an imbalance in dNTP. This will impact the DNA synthesis because the dNTP pool will be changed. The imbalanced dNTP pool leads to DNA strand breaks and to the inhibition of the DNA synthesis. Through depletion of the dNTP pool, clofarabine self-potentiates the incorporation of clofarabine triphosphates into DNA. Mitochondrion Probably hrough competitive inhibition, this drug also inhibits the DNA polymerase, the DNA ligase, and the DNA primase.
Nucleus RRM2 RRM2B SLC29A1 SLC28A2 SLC29A2 ADA DGUOK DGUOK ara-GTP ara-GTP Arranon Arranon AOT dADP H2O ADP RT H2O ara-Gua ATP ara-GMP ADP ATP ara-GDP ADP ATP ADP Na+ Na+ ORF28 LIG1 PRIM1 DNA syn