ORCID Profile
0000-0002-9511-3328
Current Organisation
University of California, San Diego
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Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587371.V1
Abstract: Supplemental Figure S1 shows expression of RBPs in healthy HSPCs and RN2c cells, sgRNA drop out dynamics in primary and secondary transplants, the molecular functions and biological processes associated with the hit RBPs and their gene essentialities.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587356
Abstract: Supplemental Figure S6 shows the GSEA of ELAVL1 depletion in mouse RN2c and human primary AML cells, ELAVL1 subcellular localization in mouse and human AML, the qRT-PCR of ELAVL1 targets in MS-444-treated RN2c cells, and the integrative analysis of the mouse RNA-seq and eCLIP-seq.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725561
Abstract: Table S8 shows transcripts from the ELAVL1 knockout RNA-sequencing data set that are (a) alternatively spliced and (b) alternatively spliced as well as bound by ELAVL1 as identified by eCLIP-sequencing.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725564
Abstract: Table S7 shows (a) reproducible peaks and (b) GO analysis of ELAVL1-bound transcripts identified in the eCLIP-sequencing data set. The negatively enriched (c) and positively-enriched (d) gene sets identified by GSEA of ELAVL1-bound and differentially expressed transcripts from the RN2c RNA-sequencing data set are shown.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725576.V1
Abstract: Table S3 shows clinical information for all AML patient specimens used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587353
Abstract: Supplemental Figure S7 shows the expression profile of TOMM34 in normal human bone marrow and across different AML and CML data sets. The effects of TOMM34 depletion on human primary AML cells in vitro and validation of TOMM34 knockdown and overexpression is shown.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587359
Abstract: Supplemental Figure S5 shows the effects of DHTS treatment on THP-1 and human primary AML cells in vitro, the effects of MS-444 treatment on human umbilical cord blood in vivo, and validation of ELAVL1 overexpression by western blot.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587362.V1
Abstract: Supplemental Figure S4 shows the validation of ELAVL1 knockdown by western blot and effects of ELAVL1 loss on human primary AML cells in vitro and in vivo.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587356.V1
Abstract: Supplemental Figure S6 shows the GSEA of ELAVL1 depletion in mouse RN2c and human primary AML cells, ELAVL1 subcellular localization in mouse and human AML, the qRT-PCR of ELAVL1 targets in MS-444-treated RN2c cells, and the integrative analysis of the mouse RNA-seq and eCLIP-seq.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725567.V1
Abstract: Table S6 shows altered gene sets identified by GSEA of the ELAVL1 knockout RN2c RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725591.V1
Abstract: Supplemental Figure S5 shows the effects of DHTS treatment on THP-1 and human primary AML cells in vitro, the effects of MS-444 treatment on human umbilical cord blood in vivo, and validation of ELAVL1 overexpression by western blot.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725582.V1
Abstract: Table S1 shows expression of RBPs in an RNA-sequencing data set of human bone marrow hematopoietic stem and progenitor subpopulations.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725558
Abstract: Table S9 shows the (a) differentially expressed transcripts and (b) altered pathways as identified by GSEA from the ELAVL1 knockdown human primary AML RNA-sequencing data set.
Publisher: Elsevier BV
Date: 1995
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587347.V1
Abstract: Table S2 shows sequences of (a) sgRNAs from the RBP screen, (b) sequencing primers, (c) shRNAs and human-targeting sgRNAs, (d) eCLIP oligos.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725570
Abstract: Table S5 shows the log2 fold change of differentially expressed transcripts from the ELAVL1 knockout RN2c RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587368
Abstract: Supplemental Figure S2 shows validation of sgRNA -mediated knockout of hit RBPs, comparison of hit RBP depletion in RN2c in vitro versus in vivo, effects of ELAVL1 loss on human AML cell lines, characteristics of the MLL-AF9 AML mouse model, and ELAVL1 expression in normal hematopoietic cells.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587368.V1
Abstract: Supplemental Figure S2 shows validation of sgRNA -mediated knockout of hit RBPs, comparison of hit RBP depletion in RN2c in vitro versus in vivo, effects of ELAVL1 loss on human AML cell lines, characteristics of the MLL-AF9 AML mouse model, and ELAVL1 expression in normal hematopoietic cells.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725576
Abstract: Table S3 shows clinical information for all AML patient specimens used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587362
Abstract: Supplemental Figure S4 shows the validation of ELAVL1 knockdown by western blot and effects of ELAVL1 loss on human primary AML cells in vitro and in vivo.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587365
Abstract: Supplemental Figure S3 shows the generation of the bcCML mouse model and the effects of ELAVL1 on normal bone marrow in vivo.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725573
Abstract: Table S4 shows limiting dilution analysis of secondary recipients transplanted with DMSO- or MS-444-treated bone marrow from primary mice
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725573.V1
Abstract: Table S4 shows limiting dilution analysis of secondary recipients transplanted with DMSO- or MS-444-treated bone marrow from primary mice
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587326.V1
Abstract: Table S9 shows the (a) differentially expressed transcripts and (b) altered pathways as identified by GSEA from the ELAVL1 knockdown human primary AML RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587353.V1
Abstract: Supplemental Figure S7 shows the expression profile of TOMM34 in normal human bone marrow and across different AML and CML data sets. The effects of TOMM34 depletion on human primary AML cells in vitro and validation of TOMM34 knockdown and overexpression is shown.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725594.V1
Abstract: Supplemental Figure S4 shows the validation of ELAVL1 knockdown by western blot and effects of ELAVL1 loss on human primary AML cells in vitro and in vivo.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587326
Abstract: Table S9 shows the (a) differentially expressed transcripts and (b) altered pathways as identified by GSEA from the ELAVL1 knockdown human primary AML RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587329
Abstract: Table S8 shows transcripts from the ELAVL1 knockout RNA-sequencing data set that are (a) alternatively spliced and (b) alternatively spliced as well as bound by ELAVL1 as identified by eCLIP-sequencing.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587332.V1
Abstract: Table S7 shows (a) reproducible peaks and (b) GO analysis of ELAVL1-bound transcripts identified in the eCLIP-sequencing data set. The negatively enriched (c) and positively-enriched (d) gene sets identified by GSEA of ELAVL1-bound and differentially expressed transcripts from the RN2c RNA-sequencing data set are shown.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587329.V1
Abstract: Table S8 shows transcripts from the ELAVL1 knockout RNA-sequencing data set that are (a) alternatively spliced and (b) alternatively spliced as well as bound by ELAVL1 as identified by eCLIP-sequencing.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725567
Abstract: Table S6 shows altered gene sets identified by GSEA of the ELAVL1 knockout RN2c RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587371
Abstract: Supplemental Figure S1 shows expression of RBPs in healthy HSPCs and RN2c cells, sgRNA drop out dynamics in primary and secondary transplants, the molecular functions and biological processes associated with the hit RBPs and their gene essentialities.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725600
Abstract: Supplemental Figure S2 shows validation of sgRNA -mediated knockout of hit RBPs, comparison of hit RBP depletion in RN2c in vitro versus in vivo, effects of ELAVL1 loss on human AML cell lines, characteristics of the MLL-AF9 AML mouse model, and ELAVL1 expression in normal hematopoietic cells.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725603
Abstract: Supplemental Figure S1 shows expression of RBPs in healthy HSPCs and RN2c cells, sgRNA drop out dynamics in primary and secondary transplants, the molecular functions and biological processes associated with the hit RBPs and their gene essentialities.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725582
Abstract: Table S1 shows expression of RBPs in an RNA-sequencing data set of human bone marrow hematopoietic stem and progenitor subpopulations.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.C.6572000.V2
Abstract: Abstract Acute myeloid leukemia (AML) is fueled by leukemic stem cells (LSC) whose determinants are challenging to discern from hematopoietic stem cells (HSC) or uncover by approaches focused on general cell properties. We have identified a set of RNA-binding proteins (RBP) selectively enriched in human AML LSCs. Using an i in vivo /i two-step CRISPR-Cas9 screen to assay stem cell functionality, we found 32 RBPs essential for LSCs in MLL-AF9 Nras sup G12D /sup AML. Loss-of-function approaches targeting key hit RBP ELAVL1 compromised LSC-driven i in vivo /i leukemic reconstitution, and selectively depleted primitive malignant versus healthy cells. Integrative multiomics revealed differentiation, splicing, and mitochondrial metabolism as key features defining the leukemic ELAVL1–mRNA interactome with mitochondrial import protein, TOMM34, being a direct ELAVL1-stabilized target whose repression impairs AML propagation. Altogether, using a stem cell–adapted i in vivo /i CRISPR screen, this work demonstrates pervasive reliance on RBPs as regulators of LSCs and highlights their potential as therapeutic targets in AML. Significance: LSC-targeted therapies remain a significant unmet need in AML. We developed a stem-cell–adapted i in vivo /i CRISPR screen to identify key LSC drivers. We uncover widespread RNA-binding protein dependencies in LSCs, including ELAVL1, which we identify as a novel therapeutic vulnerability through its regulation of mitochondrial metabolism. i a href="loodcancerdiscov/article/doi/10.1158/2643-3230.BCD-4-3-ITI" target="_blank" This article is highlighted in the In This Issue feature, p. 171 /a /i /
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725597.V1
Abstract: Supplemental Figure S3 shows the generation of the bcCML mouse model and the effects of ELAVL1 on normal bone marrow in vivo.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587335
Abstract: Table S6 shows altered gene sets identified by GSEA of the ELAVL1 knockout RN2c RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587350.V1
Abstract: Table S1 shows expression of RBPs in an RNA-sequencing data set of human bone marrow hematopoietic stem and progenitor subpopulations.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.C.6572000.V1
Abstract: Abstract Acute myeloid leukemia (AML) is fueled by leukemic stem cells (LSC) whose determinants are challenging to discern from hematopoietic stem cells (HSC) or uncover by approaches focused on general cell properties. We have identified a set of RNA-binding proteins (RBP) selectively enriched in human AML LSCs. Using an i in vivo /i two-step CRISPR-Cas9 screen to assay stem cell functionality, we found 32 RBPs essential for LSCs in MLL-AF9 Nras sup G12D /sup AML. Loss-of-function approaches targeting key hit RBP ELAVL1 compromised LSC-driven i in vivo /i leukemic reconstitution, and selectively depleted primitive malignant versus healthy cells. Integrative multiomics revealed differentiation, splicing, and mitochondrial metabolism as key features defining the leukemic ELAVL1–mRNA interactome with mitochondrial import protein, TOMM34, being a direct ELAVL1-stabilized target whose repression impairs AML propagation. Altogether, using a stem cell–adapted i in vivo /i CRISPR screen, this work demonstrates pervasive reliance on RBPs as regulators of LSCs and highlights their potential as therapeutic targets in AML. Significance: LSC-targeted therapies remain a significant unmet need in AML. We developed a stem-cell–adapted i in vivo /i CRISPR screen to identify key LSC drivers. We uncover widespread RNA-binding protein dependencies in LSCs, including ELAVL1, which we identify as a novel therapeutic vulnerability through its regulation of mitochondrial metabolism. /
Publisher: American Association for Cancer Research (AACR)
Date: 12-07-2021
DOI: 10.1158/2643-3230.22587332
Abstract: Table S7 shows (a) reproducible peaks and (b) GO analysis of ELAVL1-bound transcripts identified in the eCLIP-sequencing data set. The negatively enriched (c) and positively-enriched (d) gene sets identified by GSEA of ELAVL1-bound and differentially expressed transcripts from the RN2c RNA-sequencing data set are shown.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725585
Abstract: Supplemental Figure S7 shows the expression profile of TOMM34 in normal human bone marrow and across different AML and CML data sets. The effects of TOMM34 depletion on human primary AML cells in vitro and validation of TOMM34 knockdown and overexpression is shown.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587344.V1
Abstract: Table S3 shows clinical information for all AML patient specimens used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587338
Abstract: Table S5 shows the log2 fold change of differentially expressed transcripts from the ELAVL1 knockout RN2c RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725588.V1
Abstract: Supplemental Figure S6 shows the GSEA of ELAVL1 depletion in mouse RN2c and human primary AML cells, ELAVL1 subcellular localization in mouse and human AML, the qRT-PCR of ELAVL1 targets in MS-444-treated RN2c cells, and the integrative analysis of the mouse RNA-seq and eCLIP-seq.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725561.V1
Abstract: Table S8 shows transcripts from the ELAVL1 knockout RNA-sequencing data set that are (a) alternatively spliced and (b) alternatively spliced as well as bound by ELAVL1 as identified by eCLIP-sequencing.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587335.V1
Abstract: Table S6 shows altered gene sets identified by GSEA of the ELAVL1 knockout RN2c RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725603.V1
Abstract: Supplemental Figure S1 shows expression of RBPs in healthy HSPCs and RN2c cells, sgRNA drop out dynamics in primary and secondary transplants, the molecular functions and biological processes associated with the hit RBPs and their gene essentialities.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725579
Abstract: Table S2 shows sequences of (a) sgRNAs from the RBP screen, (b) sequencing primers, (c) shRNAs and human-targeting sgRNAs, (d) eCLIP oligos.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725570.V1
Abstract: Table S5 shows the log2 fold change of differentially expressed transcripts from the ELAVL1 knockout RN2c RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587344
Abstract: Table S3 shows clinical information for all AML patient specimens used in this study.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2033
DOI: 10.1158/2643-3230.22725594
Abstract: Supplemental Figure S4 shows the validation of ELAVL1 knockdown by western blot and effects of ELAVL1 loss on human primary AML cells in vitro and in vivo.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587347
Abstract: Table S2 shows sequences of (a) sgRNAs from the RBP screen, (b) sequencing primers, (c) shRNAs and human-targeting sgRNAs, (d) eCLIP oligos.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725591
Abstract: Supplemental Figure S5 shows the effects of DHTS treatment on THP-1 and human primary AML cells in vitro, the effects of MS-444 treatment on human umbilical cord blood in vivo, and validation of ELAVL1 overexpression by western blot.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725597
Abstract: Supplemental Figure S3 shows the generation of the bcCML mouse model and the effects of ELAVL1 on normal bone marrow in vivo.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587341
Abstract: Table S4 shows limiting dilution analysis of secondary recipients transplanted with DMSO- or MS-444-treated bone marrow from primary mice
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.C.6572000
Abstract: Abstract Acute myeloid leukemia (AML) is fueled by leukemic stem cells (LSC) whose determinants are challenging to discern from hematopoietic stem cells (HSC) or uncover by approaches focused on general cell properties. We have identified a set of RNA-binding proteins (RBP) selectively enriched in human AML LSCs. Using an i in vivo /i two-step CRISPR-Cas9 screen to assay stem cell functionality, we found 32 RBPs essential for LSCs in MLL-AF9 Nras sup G12D /sup AML. Loss-of-function approaches targeting key hit RBP ELAVL1 compromised LSC-driven i in vivo /i leukemic reconstitution, and selectively depleted primitive malignant versus healthy cells. Integrative multiomics revealed differentiation, splicing, and mitochondrial metabolism as key features defining the leukemic ELAVL1–mRNA interactome with mitochondrial import protein, TOMM34, being a direct ELAVL1-stabilized target whose repression impairs AML propagation. Altogether, using a stem cell–adapted i in vivo /i CRISPR screen, this work demonstrates pervasive reliance on RBPs as regulators of LSCs and highlights their potential as therapeutic targets in AML. Significance: LSC-targeted therapies remain a significant unmet need in AML. We developed a stem-cell–adapted i in vivo /i CRISPR screen to identify key LSC drivers. We uncover widespread RNA-binding protein dependencies in LSCs, including ELAVL1, which we identify as a novel therapeutic vulnerability through its regulation of mitochondrial metabolism. i a href="loodcancerdiscov/article/doi/10.1158/2643-3230.BCD-4-3-ITI" target="_blank" This article is highlighted in the In This Issue feature, p. 171 /a /i /
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587341.V1
Abstract: Table S4 shows limiting dilution analysis of secondary recipients transplanted with DMSO- or MS-444-treated bone marrow from primary mice
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725579.V1
Abstract: Table S2 shows sequences of (a) sgRNAs from the RBP screen, (b) sequencing primers, (c) shRNAs and human-targeting sgRNAs, (d) eCLIP oligos.
Publisher: Elsevier BV
Date: 11-2019
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725600.V1
Abstract: Supplemental Figure S2 shows validation of sgRNA -mediated knockout of hit RBPs, comparison of hit RBP depletion in RN2c in vitro versus in vivo, effects of ELAVL1 loss on human AML cell lines, characteristics of the MLL-AF9 AML mouse model, and ELAVL1 expression in normal hematopoietic cells.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587359.V1
Abstract: Supplemental Figure S5 shows the effects of DHTS treatment on THP-1 and human primary AML cells in vitro, the effects of MS-444 treatment on human umbilical cord blood in vivo, and validation of ELAVL1 overexpression by western blot.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587338.V1
Abstract: Table S5 shows the log2 fold change of differentially expressed transcripts from the ELAVL1 knockout RN2c RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725585.V1
Abstract: Supplemental Figure S7 shows the expression profile of TOMM34 in normal human bone marrow and across different AML and CML data sets. The effects of TOMM34 depletion on human primary AML cells in vitro and validation of TOMM34 knockdown and overexpression is shown.
Publisher: American Association for Cancer Research (AACR)
Date: 09-02-2023
DOI: 10.1158/2643-3230.BCD-22-0086
Abstract: LSC-targeted therapies remain a significant unmet need in AML. We developed a stem-cell–adapted in vivo CRISPR screen to identify key LSC drivers. We uncover widespread RNA-binding protein dependencies in LSCs, including ELAVL1, which we identify as a novel therapeutic vulnerability through its regulation of mitochondrial metabolism. This article is highlighted in the In This Issue feature, p. 171
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725564.V1
Abstract: Table S7 shows (a) reproducible peaks and (b) GO analysis of ELAVL1-bound transcripts identified in the eCLIP-sequencing data set. The negatively enriched (c) and positively-enriched (d) gene sets identified by GSEA of ELAVL1-bound and differentially expressed transcripts from the RN2c RNA-sequencing data set are shown.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725558.V1
Abstract: Table S9 shows the (a) differentially expressed transcripts and (b) altered pathways as identified by GSEA from the ELAVL1 knockdown human primary AML RNA-sequencing data set.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587365.V1
Abstract: Supplemental Figure S3 shows the generation of the bcCML mouse model and the effects of ELAVL1 on normal bone marrow in vivo.
Publisher: American Association for Cancer Research (AACR)
Date: 05-2023
DOI: 10.1158/2643-3230.22725588
Abstract: Supplemental Figure S6 shows the GSEA of ELAVL1 depletion in mouse RN2c and human primary AML cells, ELAVL1 subcellular localization in mouse and human AML, the qRT-PCR of ELAVL1 targets in MS-444-treated RN2c cells, and the integrative analysis of the mouse RNA-seq and eCLIP-seq.
Publisher: American Association for Cancer Research (AACR)
Date: 11-04-2023
DOI: 10.1158/2643-3230.22587350
Abstract: Table S1 shows expression of RBPs in an RNA-sequencing data set of human bone marrow hematopoietic stem and progenitor subpopulations.
Location: United States of America
No related grants have been discovered for Stefan Aigner.