Figure 6.
AK2 suppression depletes NADP/H levels in NSD2-overexpressing MM cells. (A-B) Relative quantification of NADP/H in control (shSc) and AK2-depleted (shAK2) KMS11 and KMS34-derived NSD2-high (A) and NSD2-low (B) isogenic cells. The different colors indicate different biological replicates, and the dots represent technical replicates. (C) Relative quantification of NADP/H in control and AK2-depleted NTKO cells with and without creatine (Cr; 50mM) supplementation. (D) Relative quantification of NADP/H in control and AK2-depleted TKO cells with and without cyclocreatine (cCR; 10mM) treatment. NADP/H levels were measured by enzyme-based bioluminescent assays 72 hours after IPTG-induced AK2 knockdown. Experiments were performed in biological triplicate. (E) Schematic diagram of the proposed role of AK2 in dNTP homeostasis. RNR: ribonucleotide reductase. TrxR, thioredoxin reductase; NADK: NAD+ kinase; CK, creatine kinase. ∗∗P, 0.01, ∗∗∗P, 0.001.

AK2 suppression depletes NADP/H levels in NSD2-overexpressing MM cells. (A-B) Relative quantification of NADP/H in control (shSc) and AK2-depleted (shAK2) KMS11 and KMS34-derived NSD2-high (A) and NSD2-low (B) isogenic cells. The different colors indicate different biological replicates, and the dots represent technical replicates. (C) Relative quantification of NADP/H in control and AK2-depleted NTKO cells with and without creatine (Cr; 50mM) supplementation. (D) Relative quantification of NADP/H in control and AK2-depleted TKO cells with and without cyclocreatine (cCR; 10mM) treatment. NADP/H levels were measured by enzyme-based bioluminescent assays 72 hours after IPTG-induced AK2 knockdown. Experiments were performed in biological triplicate. (E) Schematic diagram of the proposed role of AK2 in dNTP homeostasis. RNR: ribonucleotide reductase. TrxR, thioredoxin reductase; NADK: NAD+ kinase; CK, creatine kinase. ∗∗P, 0.01, ∗∗∗P, 0.001.

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