预约演示

更新于：2025-05-07

MYB x FOXM1

更新于：2025-05-07

基本信息

关联

项与 MYB x FOXM1 相关的药物

ATM-5292

靶点

FOXM1 x MYB

作用机制

FOXM1抑制剂 [+1]

在研机构

Atomic AI

原研机构

Atomic AI

在研适应症

乳腺癌 [+1]

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 MYB x FOXM1 相关的临床结果

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100 项与 MYB x FOXM1 相关的转化医学

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0 项与 MYB x FOXM1 相关的专利（医药）

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项与 MYB x FOXM1 相关的文献（医药）

2022-07-01·Gene

First report on delineation of differentially expressed genes and pathways in milk somatic cells of mastitic and healthy Murrah buffaloes

Article

作者: Arora, Reena ; Choudhary, Vikas ; Kumar, Ashish ; Ahlawat, Sonika ; Sharma, Rekha ; Chhabra, Pooja ; Kumar Vijh, Ramesh ; Kaur, Mandeep ; Singh, Tersem

Despite immense contribution of buffaloes as dairy species, limited studies have addressed the bubaline mastitis as compared to cattle. This was the first differential transcriptomic study investigating the alterations induced by clinical mastitis in buffalo milk relative to healthy controls. Comparative gene expression profiling of three biological replicates of each group identified 1014 up-regulated and 999 down-regulated genes in the diseased buffaloes (Fold change > 2, FDR < 0.05). Activation of immune and inflammatory responses were the most enriched GO terms in the mastitic animals, with higher transcript abundance of many genes coding for anti-microbial proteins such as β-defensins, perforin, granzymes, granulysin, cathelicidins etc. Analysis of the gene regulatory interactions of the up-regulated DEGs identified many hub genes that govern the cellular and macromolecular metabolic processes (E2F4, E2F1, RBL2, FOXM1, IRF1 and MYB). This study contributes to an insightful understanding of molecular mechanisms governing immune response of buffaloes to mastitis.

2020-11-05·JCI Insight1区 · 医学

MyD88/CD40 signaling retains CAR T cells in a less differentiated state

1区 · 医学

ArticleOA

作者: Krenciute, Giedre ; Fan, Yiping ; Bell, Matthew ; Gottschalk, Stephen ; Schreiner, Patrick ; Prinzing, Brooke

Chimeric antigen receptor (CAR) T cell therapy for solid tumors has shown limited efficacy in early-phase clinical studies. The majority of CARs encode CD28 and/or 41BB costimulatory endodomains, and we explored whether MyD88 and CD40 (MC) costimulatory endodomains in CARs could improve their antitumor activity. We generated CD28-, 41BB-, and MC-CAR T cells and demonstrated that MC-CAR T cells have greater proliferative capacity and antitumor activity in repeat stimulation assays and in tumor models in vivo. Transcriptomic analysis revealed that MC-CAR T cells expressed higher levels of MYB and FOXM1, key cell cycle regulators, and were activated at baseline. After stimulation, MC-CAR T cells remained in a less differentiated state than CD28- and 41BB-CAR T cells as judged by low levels of transcription factor TBET and B lymphocyte induced maturation protein 1 expression and lower cytolytic activity in comparison with CD28- and 41BB-CAR T cells. Thus, including MyD88 and CD40 signaling domains in CARs may improve current CAR T cell therapy approaches for solid tumors.

2019-12-01·BMC Medical Genomics4区 · 医学

Regulatory network analysis reveals the oncogenesis roles of feed-forward loops and therapeutic target in T-cell acute lymphoblastic leukemia

4区 · 医学

ArticleOA

作者: Wang, Yingxue ; Li, Pan ; Xia, Mengxuan ; Guo, An-Yuan ; Lei, Qian ; Zhang, Qiong ; Luo, Mei

BACKGROUNDT-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy. Aberrant expressed genes contribute to the development and progression of T-ALL. However, the regulation underlying their aberrant expression remains elusive. Dysregulated expression of transcription factors and miRNAs played important regulatory roles in the pathogenesis of T-ALL.METHODSIn this study, we analyzed the alteration of transcriptome profiling and regulatory networks between T-ALL sample and normal T cell samples at transcriptional and post-transcriptional levels.RESULTSOur results demonstrated that genes related to cell cycle and cell proliferation processes were significantly upregulated in T-ALL comparing to normal samples. Meanwhile, regulatory network analyses revealed that FOXM1, MYB, SOX4 and miR-21/19b as core regulators played vital roles in the development of T-ALL. FOXM1-miR-21-5p-CDC25A and MYB/SOX4-miR-19b-3p-RBBP8 were identified as important feed-forward loops involved in the oncogenesis of T-ALL. Drug-specific analyses showed that GSK-J4 may be an effective drug, and CDC25A/CAPN2/MCM2 could serve as potential therapeutic targets for T-ALL.CONCLUSIONSThis study may provide novel insights for the regulatory mechanisms underlying the development of T-ALL and potential therapeutic targets.

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