更新于：2024-05-01

STK33

serine/threonine kinase 33

更新于：2024-05-01

基本信息

别名

serine/threonine kinase 33、Serine/threonine-protein kinase 33、STK33

简介

Serine/threonine protein kinase which phosphorylates VIME. May play a specific role in the dynamic behavior of the intermediate filament cytoskeleton by phosphorylation of VIME (By similarity). Not essential for the survival of KRAS-dependent AML cell lines.

关联

100 项与 STK33 相关的临床结果

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100 项与 STK33 相关的转化医学

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0 项与 STK33 相关的专利（医药）

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112

项与 STK33 相关的文献（医药）

2024-02-22·The EMBO journal

Microtubule-binding protein MAP1B regulates interstitial axon branching of cortical neurons via the tubulin tyrosination cycle.

Article

作者: Jakub Ziak ; Joelle M Dorskind ; Brian Trigg ; Sriram Sudarsanam ; Xinyu O Jin ; Randal A Hand ; Alex L Kolodkin

Regulation of directed axon guidance and branching during development is essential for the generation of neuronal networks. However, the molecular mechanisms that underlie interstitial (or collateral) axon branching in the mammalian brain remain unresolved. Here, we investigate interstitial axon branching in vivo using an approach for precise labeling of layer 2/3 callosal projection neurons (CPNs). This method allows for quantitative analysis of axonal morphology at high acuity and also manipulation of gene expression in well-defined temporal windows. We find that the GSK3β serine/threonine kinase promotes interstitial axon branching in layer 2/3 CPNs by releasing MAP1B-mediated inhibition of axon branching. Further, we find that the tubulin tyrosination cycle is a key downstream component of GSK3β/MAP1B signaling. These data suggest a cell-autonomous molecular regulation of cortical neuron axon morphology, in which GSK3β can release a MAP1B-mediated brake on interstitial axon branching upstream of the posttranslational tubulin code.

2024-01-20·Pathology, research and practice

Serine/Threonine Kinase (STK) 33 promotes the proliferation and metastasis of human esophageal squamous cell carcinoma via inflammation-related pathway.

Article

作者: Haifeng Jiang ; Liping Li ; Tao Ma ; Ruixiao Wang ; Xiaozhen Chen ; Ke Xu ; Chen Chen ; Zijin Liu ; Hongmei Wang ; Lingyan Huang

The serine/threonine kinase (STK) 33 plays a key role in cancer cell proliferation and metastasis. Abnormal STK33 expression is closely related to malignancy of numerous cancers. This study suggests the important role of STK33 in the pathogenesis and metastatic progression of esophageal squamous cell carcinoma (ESCC). STK33 expression in human ESCC tissues was detected by immunohistochemical technique. Further, we analyzed the relationship between STK33 and clinical and pathological factors as well as the prognosis of patients. ECa109 cell line was cultured and transfected with STK33-RNAi lentiviral vector to perform Hochest33342 & PI and metastasis experiments. The TCGA database was used to analyze the STK33 expression level in ESCC. All statistical analyses were performed in SPSS 23.0 software. Differences with P < 0.05 were considered statistically significant. In human ESCC specimens, STK33 was overexpressed and associated with poor prognosis. Silencing STK33 expression suppressed ESCC proliferation, migration, invasion, and tumor growth. STK33 also mediated angiogenesis, TGFβ, and inflammatory response in ESCC. Mechanistic investigations revealed that STK33 regulates ESCC through multiple complex pathways. Dysregulated STK33 signaling promotes ESCC growth and progression. Thus, our findings identified STK33 as a candidate treatment target that improves ESCC therapy.

2023-11-08·The Journal of comparative neurology

Regulation of circulating thyroid hormone levels by hypothalamic tanycytes and hypophysial pars tuberalis-specific cells and their morphological and gene- and protein-expression changes under different photoperiods.

Review

作者: Yoko Kameda

Thyroid hormone in the hypothalamus acts as a key determinant of seasonal transitions. Thyroid hormone-levels in the brain are mainly regulated by the hypothalamic tanycytes and pituitary pars tuberalis (PT)-specific cells. TSHβ produced by the PT-specific cells stimulates Dio2 expression and decreases Dio3 expression of the tanycytes. Both tanycytes and PT-specific cells in photosensitive animals exhibit remarkable changes of morphological appearance and expressions of genes and proteins under different photoperiods. Long photoperiods induce increased gene- and protein-expressions and active features. Short photoperiods cause the decreased gene- and protein-expressions and inactive features. In the PT, expressions of TSHβ, common α-subunit of glycoprotein hormones (α-GSU), and MT1 receptor of melatonin receptors and eyes absent 3 change under different photoperiods. Diurnal rhythms of α-GSU mRNA expression are observed in the PT of Djungarian hamsters. Hes1, Nkx2.1, and LIM homeodomain gene 2 (Lhx2) are involved in the differentiation of PT. In the hypothalamic tanycytes, expressions of Dio2, Dio3, vimentin, serine/threonine kinase 33, GPR50, Nestin, Retinoid signaling genes (retinaldehyde dehydrogenase 1, cellular retinol binding protein 1, and Stra6), monocarboxylate transporter 8, and neural cell adhesion molecule change under different photoperiods. Rax, Lhx2, Nfia/b/x, and fibroblast growth factor 10 are involved in the differentiation of tanycytes.

项与 STK33 相关的新闻（医药）

2024-03-05

·生物制品圈

新型细胞内信号通路！宁波大学最新研究：发现“癌中之王”胰腺癌耐药机制和预后靶点

导读：胰腺导管腺癌（PDAC）的死亡率主要归因于转移和化疗耐药。近日，宁波大学研究团队在期刊《Cell Death Discovery》上在线发表题为“LncRNA MACC1-AS1 induces gemcitabine resistance in pancreatic cancer cells through suppressing ferroptosis”的研究论文，本研究发现了一种新的细胞内信号通路，在胰腺癌的吉西他滨耐药中发挥作用。通过一系列的探索和验证，这一发现可能为未来临床应用提供新的见解和理论基础。https://www.nature.com/articles/s41420-024-01866-y研究背景 01 胰腺癌是一种罕见的恶性肿瘤，仅占所有癌症病例的2%–3%。然而，它与7%的显著高死亡率相关。目前，吉西他滨是胰腺癌最常用的化疗药物。遗憾的是，吉西他滨治疗胰腺癌的总体缓解率低于20%，80%的患者在1年内复发并死亡。尽管吉西他滨在晚期转移患者中具有一定效果，但其结果并不令人满意，这主要归因于耐药性的发展。铁死亡是一种铁依赖性、脂质过氧化物积累驱动的调节性细胞死亡过程。研究表明，胰腺癌细胞利用与铁死亡相关的抗氧化系统来清除活性氧（ROS），作为逃避细胞死亡的策略。Nrf2-ARE通路在细胞抗氧化应激反应中发挥重要作用。此外，Keap1-Nrf2通路通过调节下游靶基因SLC7A11的表达水平抑制铁死亡。大量研究强调了非编码RNA，如microRNA（miRNA）和长链非编码RNA（lncRNA）在铁死亡调控中的作用。其中，MACC1-AS1已被确认为MACC1 mRNA的反义RNA。研究表明，MACC1-AS1通过腺苷活化蛋白激酶/Lin28通路稳定MACC1的表达水平，促进细胞行为，包括胃癌细胞的增殖和侵袭。尽管一些lncRNA与胰腺癌细胞的耐药性有关，但目前还没有关于MACC1-AS1与胰腺癌细胞耐药关系的研究。研究进展 02 在临床应用方面，尝试分析了胰腺癌患者中MACC1-AS1、STK33以及两者基因的表达水平及其预后意义。首先将患者分为高风险组和低风险组。然后，展示了两组的生存状态，并显示了热图，代表MACC1-AS1和MACC1-AS1+STK33的基因表达水平。KM生存曲线显示，高风险组的患者与低风险组的患者在OS、PFS和DFS率方面具有不同的中位生存时间。结果显示，MACC1-AS1的高表达表明胰腺癌患者OS、PFS和DFS的生存时间较差，但无统计学意义。然而，发现MACC1-AS1和STK33的组合对OS和PFS率均有显著影响。结果表明，MACC1-AS1和STK33的联合分析在OS和PFS方面呈现出统计学意义（P < 0.05），而对DFS仍然没有意义。此外，与单独使用基因表达相比，这种联合方法表现出更优越的性能。建立了MACC1-AS1、STK33和两者的决策曲线分析（DCA），计算了每位患者的风险评分，并使用“ggDCA” R软件包获得了不同的DCA模块。患者被分为五个模块。根据DCA分析结果，MACC1-AS1和STK33的联合预后效果表现出更高的DCA值，表明多基因模型对1年OS具有更强的预测能力。这些数据表明，MACC1-AS1和STK33可以作为胰腺癌患者临床预后的联合靶点。研究结论 03 综上所述，本研究发现了一种新的细胞内信号通路，在胰腺癌的吉西他滨耐药中发挥作用。通过一系列的探索和验证，这一发现可能为未来临床应用提供新的见解和理论基础。参考资料：https://www.nature.com/articles/s41420-024-01866-y识别微信二维码，添加生物制品圈小编，符合条件者即可加入生物制品微信群！请注明：姓名+研究方向！版权声明本公众号所有转载文章系出于传递更多信息之目的，且明确注明来源和作者，不希望被转载的媒体或个人可与我们联系(cbplib@163.com)，我们将立即进行删除处理。所有文章仅代表作者观点，不代表本站立场。

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