Ask about this productRelated genes to: STK38 Blocking Peptide
- Gene:
- STK38 NIH gene
- Name:
- serine/threonine kinase 38
- Previous symbol:
- -
- Synonyms:
- NDR, NDR1
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-19
- Date modifiied:
- 2018-05-17
Related products to: STK38 Blocking Peptide
Related articles to: STK38 Blocking Peptide
- The Hippo pathway is a key regulator of development, regeneration, tissue homeostasis, and organ size, and its dysregulation promotes tumorigenesis. However, the precise mechanisms of its regulation in both normal physiology and cancer remain incompletely understood. Here, we identify STK38 and STK38L (also known as NDR1 and NDR2), previously proposed as redundant kinases of LATS, as negative regulators of the Hippo pathway. STK38/L inhibit LATS by competitively binding to MOB1 and disrupting the LATS-MOB1 complex, a process independent of their kinase activity. This inhibitory mechanism is evolutionarily conserved, as the ortholog Tricornered similarly impairs Warts-Mats complex formation, resulting in enlarged fly wing size. Pathologically, STK38L is highly expressed in ovarian cancer and required for ovarian tumor growth, and its amplification correlates with YAP activation and increased tumor sensitivity to TEAD inhibitors. Taken together, our study reveals a conserved role of STK38/L in Hippo pathway regulation, providing new insights into Hippo-dependent growth control and cancer development. - Source: PubMed
Publication date: 2026/05/13
An JeongminHuang ZhenKizhedathu AmruthaLan TianLin TzulingJoo HyejinThilakaratne Eshan MalindaLiu YuhanXu Yun YiYang BingLara-Gonzalez PabloWarrior RahulLuo RayWang Wenqi - Alveolar type II (AT2) cells act as progenitors that sustain gas exchange and drive postinjury repair. Disruption of their proliferation-differentiation balance promotes pulmonary fibrosis and acute respiratory distress syndrome, but the core regulatory mechanisms are unclear. Serum deprivation response protein (SDPR, cavin-2), a caveolae-associated protein involved in proliferation and lipid metabolism, may modulate AT2 fate. This study investigated how the SDPR-STK38 axis regulates AT2 proliferation and differentiation and its impact on lung homeostasis and regeneration. - Source: PubMed
Publication date: 2026/05/06
Wang JieLei XuepeiHuang YiyingTang JiamingShi GuiyingLi HangBai Lin - Peutz-Jeghers syndrome (PJS) is a rare inherited cancer predisposing disorder associated with pathogenic variants of the Serine Threonine Kinase11 (STK11 / LKB1). Morbidity in children is driven by small intestinal obstruction from polyps. The molecular mechanisms driving polyp initiation and growth are poorly understood. We hypothesized that integrated phosphoproteomic analysis of pediatric Peutz-Jeghers polyps would reveal signaling networks driving polyp growth. - Source: PubMed
Publication date: 2026/05/04
Pushel IrinaRoy Badal CNolte Whitney MHarvey LisaBagherian AmberRekowski Michaella JClark Zachary DWashburn Michael PUmar ShahidAttard Thomas M - The cellular response to environmental fluctuations, such as increased temperature, is crucial in promoting cell survival and plays an increasingly recognized role in cancer biology. Important cellular functions altered by heat stress are cell polarization and protein translation. Previous studies have shown that heat stress alters the dynamics of Cdc42, a key regulator of cell polarization in eukaryotes, and promotes ribonucleoprotein (RNP) granule formation, reprogramming protein translation. The biological mechanisms underlying these vast changes are only partially known. Here, we report that the conserved NDR kinase Orb6, a homolog of mammalian STK38, responds to heat stress and regulates heat stress resilience by modulating Cdc42 dynamics and promoting RNP granule assembly in Schizosaccharomyces pombe. Also, we discovered a finely tuned mechanism whereby stress-activated mitogen-activated protein kinase (MAPK) Sty1 negatively regulates Orb6 kinase and Orb6 C-terminal phosphorylation during heat stress. Orb6 inhibition by Sty1 increases the sensitivity of the cell to heat stress in a temperature-specific manner, fostering increased stress resilience and metabolic adaptation. These observations highlight the role of NDR kinase in the process of heat adaptation and thermotolerance during environmental cell exposure to elevated temperatures. - Source: PubMed
Publication date: 2026/04/22
Doyle Laura PTams Robert NChen ChuanNuñez IllyceHaller Patrick RomanVerde Fulvia - Paligenosis is a conserved cellular plasticity program that allows mature cells to reenter the cell cycle in response to tissue injury. Paligenosis progresses via three stages: autodegradation (with dramatic increase in autophagy and lysosomes), induction of metaplastic or fetal-like genes, and cell cycle entry. Hippo signaling, particularly the downstream effector YAP1, regulates cellular plasticity, but its role in paligenosis has not been studied. Here, we examine YAP1 dynamics during paligenosis in digestive-enzyme-secreting chief cells from the mouse stomach. We identified Serine/Threonine Kinase 38 (STK38) as a noncanonical YAP1 kinase that phosphorylates and deactivates YAP1 in uninjured chief cells. During paligenosis, STK38 was degraded by autophagy in stage 1, dephosphorylating and activating YAP1. YAP1 activation was necessary and sufficient for paligenosis-driven conversion of chief cells into metaplastic, proliferating progenitors. Additionally, we show that STK38, like canonical Hippo kinases, interacts with Neurofibromatosis Type 2 (Merlin), a scaffold that recruits Hippo kinases to phosphorylate YAP1. We also observed the same pattern of YAP1 induction via autophagic destruction of STK38 in other tissues and cell types, suggesting injury-induced activation of autophagy in differentiated cells during tissue damage may be a more general feature by which Hippo effectors induce plasticity for regeneration. - Source: PubMed
Publication date: 2026/03/30
Zeng YongjiHuang Yang-ZheLi Qing KayHo RaymondBark Steven JWillet Spencer GDiPaolo Richard JMills Jason C