Ask about this productRelated genes to: MAP4K4 antibody
- Gene:
- MAP4K4 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase kinase 4
- Previous symbol:
- -
- Synonyms:
- HGK, NIK, FLH21957
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2016-10-05
Related products to: MAP4K4 antibody
Related articles to: MAP4K4 antibody
- Incorporating ultrasound (US) treatment sensitivity analysis may improve the treatment of acute myeloid leukemia (AML). - Source: PubMed
Publication date: 2026/09/07
Zhu LijiaDai Yinghua - Anthracycline induced cardiotoxicity is a significant problem for oncologists and cancer patients. The leading cause of non-cancer death in cancer patients and survivors is heart failure, which is frequently attributed to the exposure to chemotherapeutics like anthracyclines. The most notorious of these chemotherapeutics is doxorubicin, which causes cardiac contractile dysfunction, which in some cases is irreversible. In this study, we report the development of NanoDMX, a phosphatidylserine-containing liposomal formulation of DMX5804, a small molecule inhibitor of MAP4K4, and demonstrate that its administration prevents doxorubicin-induced left ventricular dysfunction in mice. Additionally, we demonstrate that DMX-5804 protects cardiomyocytes through a combination of mechanisms outside of the expected route of suppressing the JNK pathway. Overall, we demonstrate that the use of NanoDMX, a novel liposomal system using both DMX-5804 and phosphatidylserine, can prevent the damage induced by doxorubicin over the course of a single high dose model. - Source: PubMed
Publication date: 2026/08/18
Tetterton-Kellner JessicaMiserendino AudreannaTariq ImranJensen Brian CNguyen Juliane - Cancer frequently arises from the impaired functioning of the Mitogen-activated protein kinase (MAPK) signaling system, driven by mutation or overexpression of key signaling components. RAF, MEK, ERK, and KRAS inhibitors have significantly improved clinical outcomes, but efficacy is still restricted due to pathway reactivation, adaptive resistance, and signaling cross-talk. These limitations have led to the search for novel therapeutic approaches and molecular targets in the MAPK network. Melanoma, thyroid carcinoma, and pancreatic adenocarcinoma were selected because MAPK pathway alterations contribute to their pathogenesis and influence treatment response. This review examines the biological importance of MAPK signaling in these cancers and discusses MAPK-targeted therapies, mechanisms of resistance, and combination treatment options. It also addresses the expanding evidence on natural compounds that modulate MAPK- related signaling networks and reviews recent transcriptomic findings that have enhanced the identification of clinically relevant molecular targets. Additionally, MAP4K4 has been linked to tumor progression and metastasis, and poor clinical outcomes, indicating its potential as a therapeutic target for future clinical studies. The findings presented in this review suggest that combining transcriptomic evidence with molecular and pharmacological analyses could aid target prioritization and accelerate the development of targeted strategies for MAPK-driven malignancies. - Source: PubMed
Wasnik DivyaSwamy K VenkateswaraVyas Renu - As the most common malignant renal tumor in children, the progression of Wilms' tumor is frequently driven by abnormal alternative splicing (AS), cell death imbalance, and an immunosuppressive microenvironment. However, the precise regulatory chain connecting these three critical elements remains largely unexplored. This study aimed to systematically construct and characterize an "AS-cell death-immunity" regulatory network in Wilms' tumor. - Source: PubMed
Publication date: 2026/08/06
Yang ChunleiLiao ManXu HaolunWang JunBao HaibinZhang ManLi CanZheng TianLi Gang - Doxorubicin (DOX) is a highly effective chemotherapeutic agent, but its clinical application was constrained by irreversible cardiotoxicity. Increasing evidence indicates that ferroptosis is a central mechanism of DOX-induced cardiotoxicity (DIC). Both the m⁶A demethylase FTO and yes-associated protein (YAP) are found to suppress ferroptosis in DIC. Importantly, both YAP and its upstream negative regulator, MAP4K4, are potential targets of FTO. However, whether FTO regulates DOX-induced cardiac ferroptosis via the MAP4K4/YAP signaling axis remains unexplored. - Source: PubMed
Publication date: 2026/07/07
Yan YouyouSong DandanLi LongboWang Junnan