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A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response [ChIP-seq]

ABSTRACT: We assessed MLL/SET proteins and found that SETD1A is required for survival of acute myeloid leukemia (AML) cells

ORGANISM(S): Mus musculus

PROVIDER: GSE108613 | GEO | 2018/02/01

REPOSITORIES: GEO

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A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response [RNA-seq]

Project description:MLL/SET methyltransferases catalyze methylation of histone 3 lysine 4 and play critical roles in development and cancer. We assessed MLL/SET proteins and found that SETD1A is required for survival of acute myeloid leukemia (AML) cells. Mutagenesis studies and CRISPR-Cas9 domain screening, showed the enzymatic SET domain is not necessary for AML cell survival but that a newly identified region, termed the FLOS (Functional Location on SETD1A) domain, is indispensable. FLOS disruption suppresses DNA damage response genes and induces p53-dependent apoptosis. The FLOS domain acts as a Cyclin K-binding site that is required for chromosomal recruitment of Cyclin K, and for DNA repair-associated gene expression in S phase. These data identify a connection between the chromatin regulator SETD1A and the DNA damage response that is independent of histone methylation, and suggests that targeting SETD1A and Cyclin K complexes may represent a therapeutic opportunity for AML and potentially other cancers.

2018-02-01 | GSE108614 | GEO

A Non-catalytic Function of SETD1A Regulates Cyclin K and the DNA Damage Response.

Project description:MLL/SET methyltransferases catalyze methylation of histone 3 lysine 4 and play critical roles in development and cancer. We assessed MLL/SET proteins and found that SETD1A is required for survival of acute myeloid leukemia (AML) cells. Mutagenesis studies and CRISPR-Cas9 domain screening show the enzymatic SET domain is not necessary for AML cell survival but that a newly identified region termed the "FLOS" (functional location on SETD1A) domain is indispensable. FLOS disruption suppresses DNA damage response genes and induces p53-dependent apoptosis. The FLOS domain acts as a cyclin-K-binding site that is required for chromosomal recruitment of cyclin K and for DNA-repair-associated gene expression in S phase. These data identify a connection between the chromatin regulator SETD1A and the DNA damage response that is independent of histone methylation and suggests that targeting SETD1A and cyclin K complexes may represent a therapeutic opportunity for AML and, potentially, for other cancers.

| S-EPMC6052445 | biostudies-literature

A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response

Project description:A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response

| PRJNA427819 | ENA

A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-02-01 | GSE108615 | GEO

Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K. (RNA-seq)

Project description:Breast cancer is the most common cancer in women worldwide. SETD1A, a histone H3 lysine-4 methyltransferase, is associated with poor prognosis in breast cancer. While both its enzymatic and non-enzymatic functions have been implicated in cancer progression, the specific role of SETD1A in breast cancer remains unclear. This study aimed to elucidate the molecular mechanisms underlying SETD1A dependency in breast cancer.

2025-08-07 | GSE289277 | GEO

Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K. (ChIP-seq)

2025-08-07 | GSE289276 | GEO

A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response [RNA-seq]

Project description:A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response [RNA-seq]

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A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response [ChIP-seq]

Project description:A non-catalytic function of SETD1A regulates Cyclin K and the DNA damage response [ChIP-seq]

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BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (ChIP-seq)

Project description:The H3K4 methyltransferase SETD1A plays an essential role in both development and cancer. However, essential components involved in SETD1A chromatin binding remain unclear. Here, we discovered that BOD1L exhibits the highest correlated co-dependency with SETD1A in human cancer cell lines. BOD1L knockout reduces leukemia cells in vitro and in vivo, and mimics the transcriptional profiles observed in SETD1A knockout cells. The loss of BOD1L immediately reduced SETD1A distribution at transcriptional start sites (TSS) and induces transcriptional elongation defect along with the increasing of RNA polymerase II at TSS, but did not cause the reduction of H3K4me3. The Shg1 domain of BOD1L has a DNA binding ability, and recruit SETD1A to chromatin through the association with SETD1A FLOS domain. In addition, the BOD1L-SETD1A complex associates with transcriptional regulators, including E2Fs. These results reveal that BOD1L mediates chromatin and SETD1A, and regulates the non-canonical function of SETD1A in transcription.

2024-06-25 | GSE258788 | GEO

BOD1L mediates chromatin binding and non-canonical function of H3K4 methyltransferase SETD1A (RNA-seq)

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