Dataset Information

BioID of CD25 mutants in B-cell malignancies

ABSTRACT: CD25-dificient patient-derived PDX2 B-ALL cells and Jeko1 MCL cells with CRISPR-Cas9-mediated gene deletion were reconstituted with wild-type CD25 (S268) or CD25 carrying S268A mutant (A268) with C-terminal BirA (engineered biotin ligase) and selected by puromycin for 3 days. BirA expressing construct was used as negative control.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Spleen, B Cell, Bone Marrow

DISEASE(S): Acute Leukemia,Lymphoma

SUBMITTER: Mark Robinson

LAB HEAD: Markus Muschen

PROVIDER: PXD035989 | Pride | 2026-02-23

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20190122_vcs075_19-1553_Muschen_Lee_4-1.dat	Other
	20190122_vcs075_19-1553_Muschen_Lee_4-1.mgf	Mgf
	20190122_vcs075_19-1553_Muschen_Lee_4-1.raw	Raw
	20190122_vcs075_19-1553_Muschen_Lee_5-1.dat	Other
	20190122_vcs075_19-1553_Muschen_Lee_5-1.mgf	Mgf

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Publications

Dynamic feedback control of oncogenic tyrosine kinase signaling in acute leukemia.

Lee Jaewoong J Sun Ruifeng R Kume Kohei K Robinson Mark E ME Cheng Zhangliang Z Cosgun Kadriye Nehir KN Ma Ning N Hurtz Christian C Geng Huimin H Luger Selina M SM Litzow Mark R MR Paietta Elisabeth E Chen Jianjun J Vaidehi Nagarajan N Müschen Markus M

Science signaling 20260210 924

CD25 is a subunit of the interleukin-2 (IL-2) receptor on T cells and natural killer (NK) cells. Acute leukemias with oncogenic tyrosine kinases often include CD25<sup>+</sup> leukemia subpopulations, which portend poor clinical outcomes for patients; however, acute leukemia cells do not respond to IL-2. Here, we identified CD25 and its phosphorylation by protein kinase Cδ (PKCδ) as central elements of a feedback loop that stabilized fluctuations in oncogenic tyrosine kinase signaling in acute l ...[more]

PMID: 41666265

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