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Last update 08 May 2025

MAP2K5

Last update 08 May 2025

Basic Info

Synonyms

Dual specificity mitogen-activated protein kinase kinase 5, HsT17454, MAP kinase kinase 5

+ [9]

Introduction

Acts as a scaffold for the formation of a ternary MAP3K2/MAP3K3-MAP3K5-MAPK7 signaling complex. Activation of this pathway appears to play a critical role in protecting cells from stress-induced apoptosis, neuronal survival and cardiac development and angiogenesis. As part of the MAPK/ERK signaling pathway, acts as a negative regulator of apoptosis in cardiomyocytes via promotion of STUB1/CHIP-mediated ubiquitination and degradation of ICER-type isoforms of CREM (By similarity).

Drugs associated with MAP2K5

SC-1-151 (Duquesne University)

Target

MAP2K5 x MEK1 x MEK2

Mechanism

MAP2K5 inhibitors [+2]

Active Org.-

Originator Org.

Duquesne University of The Holy Spirit

Active Indication-

Inactive Indication

Triple Negative Breast Cancer

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MAP2K5

100 Translational Medicine associated with MAP2K5

0 Patents (Medical) associated with MAP2K5

488

Literatures (Medical) associated with MAP2K5

01 May 2025·Journal of Affective Disorders

Chronic inflammation response as a key factor in polycystic ovary syndrome among patients with bipolar disorder

Article

Author: Huang, Jing ; Tan, Yan ; Wu, Haishan ; Teng, Ziwei ; Chen, Gong ; Chen, Zhuohui ; Chen, Jindong ; Chen, Haiyu ; Liu, Minghui ; Liu, Jieyu ; Qin, Yue

BACKGROUNDThis study aimed to investigate serum inflammatory factor levels of polycystic ovary syndrome (PCOS) in female patients with bipolar disorder (BD) to explore the related inflammatory molecular mechanisms preliminarily.METHODSThe study recruited 72 female drug-naïve patients with BD and 98 female healthy controls (HCs). Demographic information, menstrual cycles, sex hormone levels, and ovarian ultrasound data were collected from them. Additionally, their serum inflammatory factor levels and the proteomics of peripheral blood mononuclear cells were analyzed.RESULTSThe levels of interleukin (IL)-8 and IL-13 were significantly higher in patients with BD than in HCs (p < 0.05), and the IL-8 level was higher in BD patients with PCOS than in those without (adjusted p = 0.07). Bioinformatics analysis revealed that downregulated genes with significant differences between the two groups were all involved in immune-inflammatory-related pathways, and the expression of downregulated genes BTN3A2, MAP2K5, JCHAIN-B, and DMAP1 showed substantial differences and consistent trends between the two groups.CONCLUSIONIL-8-related chronic inflammatory response is closely associated with PCOS in BD patients, and genes such as BTN3A2 may mediate this chronic inflammatory response by negatively regulating the abnormal differentiation of T helper 17 cells, serving as one of the mechanisms underlying its pathogenesis.

22 Apr 2025·Blood Advances

Targeting the RBM39-MEK5 axis synergizes with bortezomib to inhibit the malignant growth of multiple myeloma

Article

Author: Lei, Hu ; Zhang, Zilu ; Xu, Xiaoguang ; Xu, Hanzhang ; Liu, Jia ; Xu, Wenbin ; Wu, Chengyu ; Zeng, Xinyi ; Fu, Ze ; Wu, Chao ; Ye, Chenjing ; Jia, Mingyuan ; Wu, Yingli ; Yan, Hua

AbstractAberrant alternative splicing is one of the hallmarks of cancer and is potentially based on upregulated expression-of-splicing factors in some types of cancer. Our previous study suggested that the splicing factor RBM39 is significantly upregulated in multiple myeloma (MM) and that its upregulation is positively associated with poor prognosis. Here, we further demonstrate that the survival and proliferation of MM cells rely on RBM39 and that RBM39 knockdown inhibits the malignant growth of MM. Indisulam, a “molecular glue” that mediates the proteasomal degradation of RBM39, has potent suppressive effects on MM both in vitro and in vivo. Deletion of RBM39 results in extensively altered splicing, with mis-splicing of MEK5 verified to inhibit the malignant growth of MM. Full-length MEK5 plays a vital role in maintaining MM cell survival, whereas aberrant MEK5 isoforms with exon loss exhibit loss of function and a propensity for proteasomal degradation. Targeting RBM39 or MEK5 synergistically increases the cytotoxicity of bortezomib in MM cells via the inhibition of p65. Our study validates the specific mechanism of RBM39 in MM, providing an approach for broader targeting and optimized therapeutic strategies for MM.

25 Feb 2025·Journal of Experimental Botany

β-Aminobutyric acid-induced resistance in postharvest peach fruit involves interaction between the MAPK cascade and SNARE13 protein in the salicylic acid-dependent pathway

Article

Author: Li, Chunhong ; Xiang, Fei ; Zheng, Yonghua ; Yang, Sisi ; Li, Meilin ; Lei, Changyi ; Wang, Kaituo ; Zou, Yanyu

AbstractThe inducer β-aminobutyric acid (BABA) participates in the immune response in various plants. However, the specific mitogen-activated protein kinase (MAPK) cascade involved in BABA-induced resistance (BABA-IR) has not yet been elucidated. Here, peach (Prunus persica) fruits treated with the BABA exhibited pattern-triggered immunity defense against Rhizopus stolonifer, accompanied by the generation of reactive oxygen species and activation of a MAPK cascade. Transcriptome sequencing suggested that a total of 15 MAPK kinase kinase (PpMAPKKK)/MAPK kinase (PpMAPKK)/PpMAPK genes were involved in BABA-IR in peach fruit. Further qRT-PCR analysis showed that the transcript profiles of PpMAPKKK3, PpMAPKK5, and PpMAPK1 were elevated. Subsequently, yeast two-hybrid, luciferase complementation imaging, pull-down, and in vitro phosphorylation assays were conducted to characterize the complete MAPK cascade (PpMAPKKK3–PpMAPKK5–PpMAPK1) involved in peach fruit. Moreover, the downstream events of MAPK1 include the involvement of SNARE13 and the corresponding NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1)-responsive defense. Single silencing of MAPKKK3, MAPKK5, or MAPK1 and double silencing of MAPKKK3 and MAPKK5 or MAPKK5 and MAPK1 resulted in enhanced susceptibility to the fungus R. stolonifer in mutants and attenuated salicylic acid (SA)-dependent defense gene expression. In contrast, the homologous or heterologous overexpression of PpSNARE13 in peach fruit or Arabidopsis led to an enhanced SA pool and elevated expression of pathogenesis related (PR) genes. Reciprocally, the ppsnare13cas9 mutants were generally compromised in the priming of SA-dependent resistance. Therefore, the MAPKKK3–MAPKK5–MAPK1 cascade contributed to pattern-triggered immunity signal transduction in BABA-elicited peach fruit, by combination with downstream events such as SNARE13, NPR1, and SA-dependent signaling.

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MAP2K5

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