Muhammad Ahmad Maqbool

Retinal determination network reactivation drives chemoresistance and blocks myeloid differentiation in acute myeloid leukemia

Liam Clayfield, Divya Malik, Jessica S. Whittle, Jingru Xu et autres

Acute myeloid leukemia (AML) is a heterogeneous malignancy driven by abnormal transcriptional programs that block myeloid differentiation and sustain self-renewal. Despite treatment advances over the last 30 years, refractory responses remain common, underscoring the need for new therapies. Here, we reveal the …

gb, lu, fr, us (code pays fourni par la source)

The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency

Mathew Sheridan, Muhammad Ahmad Maqbool, Anne Largeot, Liam Clayfield et autres

BACKGROUND: The epigenetic factors KAT6A (MOZ/MYST3) and KMT2A (MLL/MLL1) interact in normal hematopoiesis to regulate progenitors' self-renewal. Both proteins are recurrently translocated in AML, leading to impairment of critical differentiation pathways in these malignant cells. We evaluated the potential of different KAT6A …

gb, lu, fr (code pays fourni par la source)

Figure S6 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

HMGA1 (A) and uPA/PLAU (B) mRNA levels upon depletion of p300 and/or CBP

Figure S7 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Effect of Fra-1 down-regulation on Pol II P-Ser5 and Pol II P-Ser2

Figure S4 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Contact matrices from Hi-C data from on the Chr6 33,724,700-34,948,488 region that contain the HMGA1 gene

Figure S2 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Fra-1 regulates HMGA1 expression

Figure S1 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Relative Fos family members and HMGA1 mRNAs levels in breast cancer cell lines and relative Fra-1 and Fra-2 protein levels in MDA-MB-231 cells

Table S1 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Primer and siRNA sequences

Figure S5 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Binding of AP-1 proteins to the HMGA1 locus in MDA-MB-231 cells after alteration of Fra-1 or Fra-2 levels

Figure S3 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Analysis of Fos and Jun family components binding at the HMGA1 locus according to Chip-seq data available in the ENCODE data base

Figure S3 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Analysis of Fos and Jun family components binding at the HMGA1 locus according to Chip-seq data available in the ENCODE data base

Table S1 from AP-1 Signaling by Fra-1 Directly Regulates HMGA1 Oncogene Transcription in Triple-Negative Breast Cancers

Claire Tolza, Fabienne Bejjani, Emilie Evanno, Samantha Mahfoud et autres

Primer and siRNA sequences