Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nactivation of KLF4 in T cell acute lymphoblastic leukemia promotes the expansion of leukemia cells by activating the Map2k7/Jnk pathway.

ABSTRACT: nactivation of KLF4 in T cell acute lymphoblastic leukemia promotes the expansion of leukemia cells by activating the Map2k7/Jnk pathway.

PROVIDER: PRJNA307539 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR3081553.fastq.gz	Fastqsanger.gz
	SRR3081554.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Inactivation of KLF4 in T cell acute lymphoblastic leukemia promotes the expansion of leukemia cells by activating the Map2k7/Jnk pathway. [array]

Project description:Gene expression analysis of bone marrow cells from control and Klf4 deficient T-ALL mice Deletion of Klf4 accelerates NOTCH1-induced leukemia. Analysis provides insight into function of KLF4 in leukemia.

2017-01-03 | GSE75663 | GEO

Inactivation of KLF4 in T cell acute lymphoblastic leukemia promotes the expansion of leukemia cells by activating the Map2k7/Jnk pathway. [ChIP-Seq]

Project description:Chip-Seq analysis of bone marrow cells from control and Klf4 deficient T-ALL mice

2017-01-03 | GSE76473 | GEO

nactivation of KLF4 in T cell acute lymphoblastic leukemia promotes the expansion of leukemia cells by activating the Map2k7/Jnk pathway.

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

2017-01-03 | GSE76474 | GEO

Effects of JNK on TGF-beta responses of mouse B lymphoma derived A20 cells

Project description:TGF-beta plays multiple functions in a board range of cellular responses such as proliferation, differentiation, motility and survival by activating several cellular signaling pathways, including Smads and MAP kinases (Erk, JNK and p38). In particular, TGF-beta can activate pro- or anti-apoptotic signals depending on the target cells. We found that blockage of JNK activation sensitized mouse B lymphoma derived A20 cells to TGF-beta-induced apoptosis. These results suggest that TGF-beta activate JNK to inhibit the activation of death signal that is simultaneously activated by TGF-beta. We used microarrays to gain insight into the effects of JNK inhibition on gene expression in TGF-b-stimulated A20 cells and identified JNK-dependent TGF-beta inducible genes. Keywords: time course

2007-08-01 | GSE7503 | GEO

Expression array analysis of MEC1, MEC2 and JeKo-1 cells 3h and 10h after overexpression of KLF4

Project description:In a recent study we identified the transcription factor KLF4 as deregulated by DNA methylation in chronic lymphocytic leukemia (CLL) cells in comparison to healthy B-cells. To analyze the function of KLF4 in leukemia cells and to identify downstream targets of the transcription factor we overexpressed KLF4 in 3 different cell lines: the CLL cell lines MEC1 and MEC2 and in the mantel cell lymphoma cell line JeKo-1.

2017-01-23 | GSE66514 | GEO

Novel tumor-suppressor function of KLF4 in pediatric T-cell acute lymphoblastic leukemia.

Project description:Acute lymphoblastic leukemia (ALL) is the most common hematological malignancy in pediatric patients. Despite advances in the treatment of this disease, many children with T-cell ALL (T-ALL) die from disease relapse due to low responses to standard chemotherapy and the lack of a targeted therapy that selectively eradicates the chemoresistant leukemia-initiating cells (LICs) responsible for disease recurrence. We reported recently that the reprogramming factor Krüppel-like factor 4 (KLF4) has a tumor-suppressive function in children with T-ALL. KLF4 silencing by promoter deoxyribonucleic acid (DNA) methylation in patients with T-ALL leads to aberrant activation of the mitogen-activated protein kinase kinase MAP2K7 and the downstream c-Jun NH2-terminal kinase (JNK) pathway that controls the expansion of leukemia cells via c-Jun and activating transcription factor 2. This pathway can be inhibited with small molecules and therefore has the potential to eliminate LICs and eradicate disease in combination with standard therapy for patients with refractory and relapsed disease. The present review summarizes the role of the KLF4-MAP2K7 pathway in T-ALL pathogenesis and the function of JNK and MAP2K7 in carcinogenesis and therapy.

| S-EPMC5568468 | biostudies-literature

Klf4

Project description:Klf4 is the zinc finger transcription factor indispensable for terminal maturation of epithelial tissues and part of group of proteins for the generation of pluripotent embryonic stem cells from differentiated tissues. No definitive in-vivo-function of Klf4 in the hematopoietic system has been established yet. We show here that Klf4 directly guides the transcriptional program for terminal differentiation of Ly-6Chigh monocytes. Klf4 suppresses transcripts of the interferon immune response and induces a proinflammatory cytokine transcriptional program. Concordantly, Klf4 hematopoietic deficiency in mice results in an enhanced Th1 but impaired Th17 immune response, and, consequently, those mice are resistant towards the induction of experimental autoimmune encephalitis (EAE). We here identify Klf4 is a transcription factor required for ontogenesis and function of Ly-6Chigh monocytes at the interface of innate and acquired immunity.

2012-07-31 | GSE11572 | GEO

KMT2A-rearranged leukemia proteomics

Project description:Activating mutations in kinase/PI3K/RAS signaling pathways are common in acute leukemia with KMT2A rearrangements (KMT2A-R). These mutations are often subclonal and their biological impact remain unclear. Using a retroviral acute myeloid leukemia model, we demonstrate that NRASG12D, FLT3ITD, and FLT3N676K accelerates KMT2A-MLLT3 leukemia onset. Importantly, also the presence of subclonal FLT3N676K in KMT2A-R leukemic cells shorten disease latency, possibly by providing stimulatory factors such as Mif. Acquired de novo mutations in Braf, Cbl, Kras, and Ptpn11 were identified in KMT2A-MLLT3 driven leukemia and favored clonal expansion. KMT2A-MLLT3 leukemia with an activating mutation enforce Myc- and Myb transcriptional modules, whereas KMT2A-MLLT3 leukemias lacking activating mutations displayed upregulation of signal transduction pathways. Our results provide new insight into the biology of KMT2A-R leukemia and highlights the importance of activated signaling as a contributing driver in this disease.

2018-05-02 | PXD008213 | Pride

Activated interleukin-7 receptor signaling drives B-cell acute lymphoblastic leukemia in mice

Project description:Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a high-risk subtype of B-ALL often associated with genetic variants that alter cytokine receptor signaling, including mutations in the interleukin-7 receptor (IL7R). To investigate whether IL7R variants are leukemia-initiating, we built mouse models expressing activated Il7r (aIL7R). B-cell intrinsic aIL7R mice developed spontaneous B-ALL, demonstrating sufficiency of Il7r activating mutations in leukemogenesis. Concomitant introduction of a knock-out allele in the associated adapter protein Lnk (encoded by Sh2b3) or a dominant-negative variant of the transcription factor Ikaros (Ikzf1) increased disease penetrance. The resulting murine leukemias displayed monoclonality and recurrent somatic Kras mutations and efficiently engrafted into immunocompetent mice. Phosphoproteomic analyses of aIL7R leukemic cells revealed constitutive Stat5 signaling and B cell receptor (BCR)-like signaling despite absence of surface pre-BCR. Finally, in vitro treatment of aIL7R leukemic B-cells with Jak, mTOR, or Syk inhibitors blocked growth, confirming that each pathway is active in this mouse model of IL7R-driven B-ALL

2021-06-28 | PXD026438 | Pride

Activated interleukin-7 receptor signaling drives B-cell acute lymphoblastic leukemia in mice

2021-06-28 | PXD026322 | Pride