Evidence map›Paper›PMID 39150611›Full record

ArticleGenes & genomics2024

A novel study on CXXC5: unraveling its regulatory mechanisms in hematopoietic stem cell biology through proteomics and gene editing.

Shanshan Liu, Yan Gao, Xianqi Feng, Yujie Xu, Minghui Hu, Hairong Fei, Hongying Zheng, Junxia Huang, Tianlan Li, Chunting Zhao and 1 more

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Article in Genes & genomics, 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. Signal integrator function of CXXC5 in Cancer.Cell communication and signaling : CCS · 2025
    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

11 authors.

Shanshan LiuDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China.
Yan GaoDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China.
Xianqi FengDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China.
Yujie XuDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China.
Minghui HuClinical Lab, The Affiliated Hospital of Qingdao University, Qingdao, China.
Hairong FeiDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China.
Hongying ZhengClinical Lab, The Affiliated Hospital of Qingdao University, Qingdao, China.
Junxia HuangDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China.
Tianlan LiDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China.
Chunting ZhaoDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China. ctzhao-006@medmail.com.cn.
Lingjie SunDepartment of Hematology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Shinan District, Qingdao, Shandong Province, China. lingjie114@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study investigates the role of CXXC5 in the self-renewal and differentiation of hematopoietic stem cells (HSCs) within the bone marrow microenvironment, utilizing advanced methodologies such as single-cell RNA sequencing (scRNA-seq), CRISPR-Cas9, and proteomic analysis.

methodsWe employed flow cytometry to isolate HSCs from bone marrow samples, followed by scRNA-seq analysis using the 10x Genomics platform to examine cell clustering and CXXC5 expression patterns. CRISPR-Cas9 and lentiviral vectors facilitated the knockout and overexpression of CXXC5 in HSCs. The impact on HSCs was assessed through qRT-PCR, Western blot, CCK-8, CFU, and LTC-IC assays, alongside flow cytometry to measure apoptosis and cell proportions. A mouse model was also used to evaluate the effects of CXXC5 manipulation on HSC engraftment and survival rates.

resultsOur findings highlight the diversity of cell clustering and the significant role of CXXC5 in HSC regulation. Knockout experiments showed reduced proliferation and accelerated differentiation, whereas overexpression led to enhanced proliferation and delayed differentiation. Proteomic analysis identified key biological processes influenced by CXXC5, including cell proliferation, differentiation, and apoptosis. In vivo results demonstrated that CXXC5 silencing impaired HSC engraftment in a bone marrow transplantation model.

conclusionCXXC5 is crucial for the regulation of HSC self-renewal and differentiation in the bone marrow microenvironment. Its manipulation presents a novel approach for enhancing HSC function and provides a potential therapeutic target for hematological diseases.

Indexed as

Cell DifferentiationGene EditingHematopoietic Stem CellsProteomicsTranscription FactorsAnimalsApoptosisCell ProliferationCRISPR-Cas SystemsDNA-Binding ProteinsHumansMiceMice, Inbred C57BLCXXC5 protein, humanDNA-Binding ProteinsTranscription FactorsBone marrow microenvironmentCell differentiationCRISPR-Cas9CXXC5Hematopoietic stem cellsProteomicsSelf-renewalSingle-cell RNA sequencing

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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.