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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 2-chloro-2′-deoxyadenosine 5′-triphosphate 2-chloro-2′-deoxyadenosine 5′-triphosphate dADP Cladribine Cladribine an oxidized thioredoxin H2O ADP reduced thioredoxin Na+ Na+ Nucleoside Salvage Pathway DNA polymerase catalytic subunit Fe2+ DNA synthesis DNA strand breaks Cytosol Cladribine is converted to its monophosphate, diphosphate and, finally, its triphosphate forms in the nucleoside salvage pathway. T or B Cell Blood vessel T or B Cell Apoptosis The apoptosis of the T and B cells results in the immunosuppression of the patient by the death of the B and T cells and, also, by the arrest of antibodies production. Due to the DNA strand breaks and the inhibition of the DNA synthesis, the T and B cells will go through apoptosis.This drug cause cells to accumulate at the G1/S phase junction. 2-chloro-2′-deoxyadenosine 5′-triphosphate accumulates and is incorporated in the DNA due to its structure. Through competitive inhibition, this drug also inhibits the DNA polymerase. Nucleus The presence of the chlorine atom at position 2 of the purine ring makes the molecule resistant to the enzymatic degradation by the adenosine desaminase. This results in its accumulation. The incorporation in the DNA results in DNA breakages 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 2-chloro-2′-deoxyadenosine 5′-triphosphate 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 the PARP activation and the glycolysis inhibition, it produces the ATP depletion, leading to the cell death.
Nucleus RRM2 RRM2B SLC29A1 SLC28A2 SLC29A2 2-chloro-2′- deoxyadenosine 5′-triphosphate 2-chloro-2′- deoxyadenosine 5′-triphosphate dADP Cladribine Cladribine an oxidized thioredoxin Water Adenosine diphosphate reduced thioredoxin Sodium Sodium Nucleoside Salvage Pathway UL30 DNA synthesis DNA strand breaks
RRM2 RRM2B SLC29A1 SLC28A2 SLC29A2 CdATP CdATP dADP 2-Cda 2-Cda AOT H2O ADP RT Na+ Na+ Nu Sa P UL30 Fe2+ DNA syn DN st b Cytosol Cladribine is converted to its monophosphate, diphosphate and, finally, its triphosphate forms in the nucleoside salvage pathway. T or B Cell Blood vessel T or B Cell Apoptosis The apoptosis of the T and B cells results in the immunosuppression of the patient by the death of the B and T cells and, also, by the arrest of antibodies production. Due to the DNA strand breaks and the inhibition of the DNA synthesis, the T and B cells will go through apoptosis.This drug cause cells to accumulate at the G1/S phase junction. 2-chloro-2′-deoxyadenosine 5′-triphosphate accumulates and is incorporated in the DNA due to its structure. Through competitive inhibition, this drug also inhibits the DNA polymerase. Nucleus The presence of the chlorine atom at position 2 of the purine ring makes the molecule resistant to the enzymatic degradation by the adenosine desaminase. This results in its accumulation. The incorporation in the DNA results in DNA breakages 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 2-chloro-2′-deoxyadenosine 5′-triphosphate 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 the PARP activation and the glycolysis inhibition, it produces the ATP depletion, leading to the cell death.
Nucleus RRM2 RRM2B SLC29A1 SLC28A2 SLC29A2 CdATP CdATP dADP 2-Cda 2-Cda AOT H2O ADP RT Na+ Na+ Nu Sa P UL30 DNA syn DN st b