Evidence map›Paper›PMID 38871923›Full record

ArticleActa pharmacologica Sinica2024

HBXIP induces PARP1 via WTAP-mediated m

Xue-Li Fu, Shi-Man Guo, Jia-Qi Ma, Fang-Yuan Ma, Xue Wang, Yan-Xin Tang, Ye Li, Wei-Ying Zhang, Li-Hong Ye

Abstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Unveiling the dynamics and therapeutic potential of mInternational journal of biological sciences · 2025
    Review
  5. Increased expression ofTranslational cancer research · 2024
    Article
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

9 authors.

Xue-Li FuState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Shi-Man GuoState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Jia-Qi MaState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Fang-Yuan MaState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Xue WangState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Yan-Xin TangState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Ye LiState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China.
Wei-Ying ZhangState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China. zhwybao@nankai.edu.cn.
Li-Hong YeState Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Sciences, Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, 300071, China. yelihong@nankai.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poly (ADP-ribose) polymerase 1 (PARP1) is a DNA-binding protein that is involved in various biological functions, including DNA damage repair and transcription regulation. It plays a crucial role in cisplatin resistance. Nevertheless, the exact regulatory pathways governing PARP1 have not yet been fully elucidated. In this study, we present evidence suggesting that the hepatitis B X-interacting protein (HBXIP) may exert regulatory control over PARP1. HBXIP functions as a transcriptional coactivator and is positively associated with PARP1 expression in tissues obtained from hepatoma patients in clinical settings, and its high expression promotes cisplatin resistance in hepatoma. We discovered that the oncogene HBXIP increases the level of PARP1 m

Indexed as

Carcinoma, HepatocellularCCAAT-Enhancer-Binding ProteinsCisplatinDrug Resistance, NeoplasmLiver NeoplasmsPoly (ADP-Ribose) Polymerase-1Adaptor Proteins, Signal TransducingAdenosineAnimalsAntineoplastic AgentsCell Line, TumorGene Expression Regulation, NeoplasticHep G2 CellsHumansMiceMice, NudeAdaptor Proteins, Signal TransducingAdenosineAntineoplastic AgentsCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanCisplatinLAMTOR5 protein, humanN-methyladenosinePARP1 protein, humanPoly (ADP-Ribose) Polymerase-1cisplatin resistanceHBXIPhepatomam6APARP1

Identifiers

PMID38871923
PMCPMC11489769

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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.