Hap1 wt

Manufactured by Horizon Discovery

HAP1 WT is a cell line derived from the near-haploid human chronic myelogenous leukemia (CML) cell line KBM-7. It is a widely used research tool for genetic studies and functional genomics.

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Lab products found in correlation

Hek293t, by American Type Culture Collection (1 mentions) Cal 51, by Leibniz Institute DSMZ (1 mentions) Mda mb 436, by American Type Culture Collection (1 mentions) Mycoalert, by Lonza (1 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (1 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (1 mentions)

2 protocols using hap1 wt

Cell lines for BRCA2 and SIRT studies

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DLD1 BRCA2^+/+ and ^–/– (Horizon Discovery), HAP1 WT, SIRT1^–/–, SIRT3^–/–, SIRT6^–/– (Horizon Discovery), CAL51 (DSMZ), HEK293T, MDA-MB-436 (ATCC) and U2OS WT and U2OS HPF1^–/– (gift from Ivan Ahel) cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% FBS (with 10 µg/ml insulin in the case of MDA-MB-436). SUM149 cells (Asterand Bioscience) were maintained in Ham’s F-12 medium supplemented with 5% FBS, 10 µg/ml insulin and 1 µg/ml hydrocortisone.
All human cell line identities were confirmed by STR typing and verified free of mycoplasma infection using Lonza MycoAlert.

Bajrami I., Walker C., Krastev D.B., Weekes D., Song F., Wicks A.J., Alexander J., Haider S., Brough R., Pettitt S.J., Tutt A.N, & Lord C.J. (2021). Sirtuin inhibition is synthetic lethal with BRCA1 or BRCA2 deficiency. Communications Biology, 4, 1270.

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Culturing HAP1 Cell Lines

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HAP1 WT (item #C631 bath 29663) and HAP1 Human SNCA 103bp deletion knockout (item #HZGHC003210c003 batch 2) cell lines were purchased from Horizon Discovery. Cells were maintained at 37C 5% CO2 and grown in IMDM media (Gibco #11995–065)+10% Fetal Bovine Serum +5% penicillin-streptomycin (Gibco #1514022). Cells were passed when ~75% confluent and discarded above passage number 10.

Rose E.P., Osterberg V.R., Banga J.S., Gorbunova V, & Unni V.K. (2024). Alpha-synuclein regulates the repair of genomic DNA double-strand breaks in a DNA-PKcs-dependent manner. bioRxiv.

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