Ask about this productRelated genes to: MKNK2 Blocking Peptide
- Gene:
- MKNK2 NIH gene
- Name:
- MAPK interacting serine/threonine kinase 2
- Previous symbol:
- GPRK7
- Synonyms:
- MNK2
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-29
- Date modifiied:
- 2019-04-12
Related products to: MKNK2 Blocking Peptide
Related articles to: MKNK2 Blocking Peptide
- Mitogen-activated protein kinase-interacting kinase 1 and 2 (MNK1/2) regulate the phosphorylation of eukaryotic translation initiation factor 4E (eIF4E), which is critical for mRNA translation initiation. Herein, we reported the discovery and development of a series of furo[3,2-c]pyridine-containing compounds, exhibiting nanomolar potency against both MNK1 and MNK2. A representative compound 34 displayed potent MNK1 and MNK2 inhibitory activity (MNK1/2 IC = 1.2/1.3 nM) with high selectivity. This compound reduced the phosphorylation of eIF4E and decreased the expression of Mcl-1 and Cyclin D1 in CT26 colorectal tumor cells. Oral administration of 34 alone inhibited tumor growth in CT26 mouse model. Moreover, the combination of 34 with anti-mPD-1 antibody achieved a superior antitumor effect with increased CD8 T cell infiltration. Overall, this work identifies a promising lead compound for the development of MNK inhibitors as small-molecule therapeutics against colorectal cancer. - Source: PubMed
Publication date: 2026/04/11
Yuan XinruiWang ZeruCui XihanXia WenjingLiu YimingSun ZijiePei YifengGuan DezhongXu HongyanHu LeiYang Chao-YieZhang Huibin - Poorly differentiated endometrial carcinoma in Black African women is under-characterized at the transcriptomic level, although it is known for aggressive subtypes. We conducted the first RNA-seq analysis of formalin-fixed, paraffin-embedded (FFPE) tumors from Black South African women to explore population-specific gene expression, alternative splicing, and novel isoforms. - Source: PubMed
Publication date: 2026/03/24
Molefi ThuloAlaouna MohammedChipiti TalentSebitloane HannahDlamini Zodwa - Provirus integration in Moloney murine leukemia virus (Pim) and mitogen-activated protein kinase-interacting kinase (Mnk) cooperatively activate the cap-dependent protein translation and are being used as targets to develop anticancer agents. We reported the first dual Pim/Mnk inhibitor with a pyrido[3,2-]pyrimidine core. We optimized the properties of through bioisostere replacement and synthesized a new group of compounds. Among these compounds, exhibited improved selectivity and kinase inhibition activities, with IC values of 32, 3, and 37 nM against Mnk1, Mnk2, and Pim1, respectively. displayed better antiproliferative effects in leukemia cell lines with cell cycle arrest and apoptosis induction. Western blot analysis revealed that decreased the levels of Mnk substrate p-eIF4E and Pim substrate p-4EBP1 in leukemia cell lines. exhibited improved water solubility and pharmacokinetic profile with potent antileukemia effects in MOLM-13 xenografts. emerges as a novel dual Pim/Mnk inhibitor with potential for further development as an antileukemic agent. - Source: PubMed
Publication date: 2026/03/24
Xing KunLi ShujunZuo ShuweiZhang HuiminZhang FuyaoLi JinghuanWen JiachenLiu DanWaxman SamuelJing YongkuiHuang MinZhang JingyiZhao Linxiang - Myasthenia gravis (MG) is an autoimmune disorder in which circular RNAs (circRNAs) are increasingly implicated, with growing evidence supporting their critical role in autoimmune pathogenesis. The role of hsa_circ_0000313 in MG, including its biological functions and mechanisms, remains unknown. - Source: PubMed
Li YingKong XiaotongCai HanluTian WenqiRen YingjieXu FanfanPeng ShanshanNiu JingyanXin GuanghaoWang JianjianZhang HuixueWang Lihua - Multiple p38 MAP kinase inhibitors have been developed for the treatment of inflammatory diseases such as rheumatoid arthritis, but their effectiveness has been limited due to toxicity and tachyphylaxis, leading to a lack of clinical benefit. Efforts have been made to circumvent this limitation by targeting individual substrates downstream of p38, including MK2 and MK5. This approach has failed to yield clinical benefit despite preclinical evidence of a therapeutic effect. We hypothesized that there is redundancy in the MAPK activating kinase family that would necessitate blocking multiple kinases to sufficiently impact inflammatory processes. We used heterobifunctional protein degraders that either specifically degraded MK2 selectively or degraded MK2/3/5 simultaneously to test the hypothesis, in addition to genetic approaches to enable knockdown. In human PBMCs, elimination of MK2/3/5 with heterobifunctional degraders resulted in full reduction of TLR4 or TLR7/8 induced TNFα, whereas MK2-specific degradation only attenuated TNFα biosynthesis. In contrast, both specific MK2 degradation and broad MK2/3/5 degradation inhibited TGF-β-induced collagen production in human fibroblasts. This observation was consistent with genetic deletions of MK2, MK3 and MK5 (singly and in combination) whereby single deletion of MK2, MK3 or MK5 attenuated lipopolysaccharide (LPS) induced TNFα production and had no effect on R848-induced TNFα production. Double deletion of MK2 and MK3 or MK2 and MK5 or MK2/3/5 triple deletion had a significantly greater effect on TNFα production regardless of stimulus. The combined data suggest cooperativity between MK2 and either MK3 or MK5 for efficient, cell context-dependent modulation of inflammatory responses. - Source: PubMed
Publication date: 2026/01/14
Yang BinFang GuoqiangMarx IsaacLiu GuangSkouras StephanieSharma KirtiWalther Dirk MBollinger Martinez SarahHubeau CedricShi YataoDe Savi ChrisHuang XinHuhn AnnissaSawant RupaProctor William RDixit Vaishali SDong HuijunWeiss Matthew MMainolfi NelloSlavin AnthonyLong Andrew JWilliams Juliet AByrne Fergus R