Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The bcl6 corepressor mutation regulates the progression and transformation of myelodysplastic syndromes by repressing the autophagy flux.

The international journal of biochemistry & cell biology - 1 Dec 2023

Chen Jia-Nan, Jin Jia-Cheng, Guo Juan, Tao Ying, Xu Fan-Huan, Liu Qi, Li Xiao, Chang Chun-Kang, Wu Ling-Yun

Abstract excerpt

The occurrence of autophagy dysregulation is vital in the development of myelodysplastic syndrome and its transformation to acute myeloid leukemia. However, the mechanisms are largely unknown. Here, we have investigated the mechanism of the bcl6 corepressor mutation in myelodysplastic syndrome development and its transformation to acute myeloid leukemia. We identified a novel pathway involving histone deacetylase...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy
Share to Co-Repressor Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Leukemia, Myeloid, Acute

Share to Mutation

Share to Myelodysplastic Syndromes

Share to Transcription Factors

Source

Identifiers

PMID: 37884171
DOI: 10.1016/j.biocel.2023.106480

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The bcl6 corepressor mutation regulates the progression and transformation of myelodysplastic syndromes by repressing the autophagy flux.PMID 37884171Read ↗

Autophagy in the pathogenesis of myelodysplastic syndrome and acute myeloid leukemiaSemantic proximity Read ↗

How recent advances in high-risk myelodysplastic syndrome physiopathology may impact future treatments.Semantic proximity Read ↗

Molecular mechanisms of the progression of myelodysplastic syndrome to secondary acute myeloid leukaemia and implication for therapySemantic proximity Read ↗

U2AF1 mutation promotes tumorigenicity through facilitating autophagy flux mediated by FOXO3a activation in myelodysplastic syndromes.Semantic proximity Read ↗

CircZBTB46 Protects Acute Myeloid Leukemia Cells from Ferroptotic Cell Death by Upregulating SCDSemantic proximity Read ↗

SETBP1 mutations drive leukemic transformation in ASXL1-mutated MDS.Semantic proximity Read ↗

Targeting lysine demethylase 6B ameliorates ASXL1 truncation–mediated myeloid malignancies in preclinical modelsSemantic proximity Read ↗

Somatic mutations of activating signalling, transcription factor, and tumour suppressor are a precondition for leukaemia transformation in myelodysplastic syndromes.Semantic proximity Read ↗

Elevated serum direct bilirubin is predictive of a poor prognosis for primary myelodysplastic syndrome.Semantic proximity Read ↗

Somatic mutations of activated signaling genes, transcription factors, or tumor suppressors are a precondition for leukemic transformation from myelodysplastic syndromes: a sequencing analysis of 64 paired samplesSemantic proximity Read ↗

Bcor insufficiency promotes initiation and progression of myelodysplastic syndromeSemantic proximity Read ↗

p62/SQSTM1 in cancer: phenomena, mechanisms, and regulation in DNA damage repairSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.