Evidence map›Paper›PMID 39017847›Full record

ReviewAdvances in experimental medicine and biology2024

Transcription Factor TAL1 in Erythropoiesis.

Johannes Fechner, Jörn Lausen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Immunoregulation role of the erythroid cells.Frontiers in immunology · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Johannes FechnerDepartment of Eukaryotic Genetics, Institute of Biomedical Genetics, University of Stuttgart, Stuttgart, Germany.
Jörn LausenDepartment of Eukaryotic Genetics, Institute of Biomedical Genetics, University of Stuttgart, Stuttgart, Germany. joern.lausen@ibmg.uni-stuttgart.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lineage-specific transcription factors (TFs) regulate differentiation of hematopoietic stem cells (HSCs). They are decisive for the establishment and maintenance of lineage-specific gene expression programs during hematopoiesis. For this they create a regulatory network between TFs, epigenetic cofactors, and microRNAs. They activate cell-type specific genes and repress competing gene expression programs. Disturbance of this process leads to impaired lineage fidelity and diseases of the blood system. The TF T-cell acute leukemia 1 (TAL1) is central for erythroid differentiation and contributes to the formation of distinct gene regulatory complexes in progenitor cells and erythroid cells. A TAL1/E47 heterodimer binds to DNA with the TFs GATA-binding factor 1 and 2 (GATA1/2), the cofactors LIM domain only 1 and 2 (LMO1/2), and LIM domain-binding protein 1 (LDB1) to form a core TAL1 complex. Furthermore, cell-type-dependent interactions of TAL1 with other TFs such as with runt-related transcription factor 1 (RUNX1) and Kruppel-like factor 1 (KLF1) are established. Moreover, TAL1 activity is regulated by the formation of TAL1 isoforms, posttranslational modifications (PTMs), and microRNAs. Here, we describe the function of TAL1 in normal hematopoiesis with a focus on erythropoiesis.

Indexed as

ErythropoiesisT-Cell Acute Lymphocytic Leukemia Protein 1AnimalsCell DifferentiationHematopoietic Stem CellsHumansProto-Oncogene ProteinsProto-Oncogene ProteinsTAL1 protein, humanT-Cell Acute Lymphocytic Leukemia Protein 1Epigenetic regulationErythropoiesisGene regulationHematopoiesisMicroRNAPosttranslational modificationProtein isoformTAL1Transcription factor

Identifiers

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.