Proteomics

Dataset Information

0

LMO2/LDB1 protein complex in AML cells


ABSTRACT: These are raw mass spectrometry data discussed in our paper: “The LMO2-LDB1-TAL1 complex regulates transcription networks in AML”, where we implicate this multisubunit complex as a key regulator of leukemia cell transcription. The key method was affinity purification followed by tandem mass spectrometry. The LDB1 and LMO2 proteins were FLAG tagged and encoding cDNAs were cloned into lentiviral expression vectors allowing transduction of leukemia cells. Protein purification and MS/MS are described below.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Suspension Culture, Permanent Cell Line Cell

DISEASE(S): Acute Leukemia

SUBMITTER: Utpal Dave  

LAB HEAD: Utpal Dave

PROVIDER: PXD068576 | Pride | 2026-02-09

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
checksum.txt Txt
pEX1_klr_5898_20210612_14.raw Raw
pEX1_klr_5898_20210612_16.raw Raw
pEX1_klr_5898_20210612_18.raw Raw
pEX1_klr_5898_20210612_2.raw Raw
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Publications

The LMO2-LDB1-TAL1 complex regulates transcription networks in acute myeloid leukemia.

Dunham Nicholas N   Wang Zhenjia Z   Neelamraju Yaseswini Y   Guo Yan Y   Paudel B Bishal BB   Meydan Cem C   Gandara Jorge A JA   Abdelmalak Fady A FA   Fan Hao H   Hardwick Joyce J   Layer Justin H JH   Lee Tak T   Maier Bernhard B   McDonald W Hayes WH   Patnaik Isaani I   Prajapati Subhash S   Rapaport Franck F   Sheridan Caroline C   Sheynkman Gloria G   Zumbo Paul P   Becker Michael W MW   Bullinger Lars L   Carroll Martin P MP   D'Andrea Richard J RJ   Dillon Richard R   Levine Ross L RL   Mason Christopher E CE   Melnick Ari M AM   Neuberg Donna S DS   Bekiranov Stefan S   Zang Chongzhi C   Davé Utpal P UP   Garrett-Bakelman Francine E FE  

Blood neoplasia 20251125 1


Relapsed acute myeloid leukemia (relAML) remains a clinical challenge. We have shown that epigenetic heterogeneity may contribute to transcriptional dysregulation and disease progression in AML, but the specific aberrant transcriptional programs have not been identified. We analyzed molecular profiles from patient-matched diagnostic and relapse AML specimens. A subset of differentially expressed genes (DEG) that were disparate in direction of expression change identified 2 patient subtypes. We p  ...[more]

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