Ask about this productRelated genes to: LATS1 antibody
- Gene:
- LATS1 NIH gene
- Name:
- large tumor suppressor kinase 1
- Previous symbol:
- -
- Synonyms:
- WARTS
- Chromosome:
- 6q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-18
- Date modifiied:
- 2014-11-19
Related products to: LATS1 antibody
Related articles to: LATS1 antibody
- Gypensapogenin I (GI) is a new dammarane type triterpenoid saponin extracted from Gynostemma pentaphyllum. This study explored the therapeutic potential and mechanism of GI on liver fibrosis (LF). LF is a key pathological stage of chronic liver disease, and the current treatment is limited. In the mouse LF model induced by carbon tetrachloride (CCl) and the LX-2 hepatic stellate cell model activated by transforming growth factor-β1 (TGF-β1), GI showed significant antifibrotic effects in vitro and in vivo, and could reduce liver injury, inflammation, collagen deposition and cell activation. Mechanistic studies have shown that GI exerts its effect by directly targeting MST1 protein. The direct and specific interaction between GI and MST1 was confirmed by surface plasmon resonance (SPR), drug affinity reaction target stability (DARTS) and cell thermal transition analysis (CETSA). Site directed mutagenesis further identified Arg181 as a key residue necessary for the stable binding of GI to MST1. This binding activated the Hippo signaling pathway, promoted the phosphorylation of MST1, LATS1/2 and YAP, resulting in the retention and inactivation of YAP in the cytoplasm. More importantly, after knockdown of STK4 gene encoding Mst1 by siRNA, the antifibrotic effect of GI was completely abolished, thus establishing MST1 as its essential functional target. In summary, this study found that GI is a novel MST1 agonist, which alleviates LF by targeting Arg181 residue, restoring Hippo/YAP pathway homeostasis and inhibiting hepatic stellate cell activation, which makes GI a promising candidate drug in the treatment of LF. - Source: PubMed
Huang KexinChen XiaoxuPei HanboYang NanMiao YuxinZhang XiaoshuYue Jiayin - High glucose-induced injury to human retinal endothelial cells (HRCCs) is closely associated with retinal disorders, and melatonin has potential protective effects. However, its underlying mechanism remains unclear. - Source: PubMed
Publication date: 2026/09/08
Mao ZiqingYou Zhipeng - Facial retaining ligaments maintain soft-tissue position and support the lower face, but whether fractional subnanosecond Nd:YAG laser treatment can improve the matrix architecture of ultraviolet (UV)-aged ligament tissue remains unclear. We evaluated whether laser-associated matrix alteration was accompanied by coordinated changes in LATS1-YAP-IQGAP1-NFAT1 signaling and collagen type I-dominant remodeling. Male Sprague-Dawley rats were allocated to non-UV control, UV-aged, and UV-aged plus laser groups ( = 5 per group). After UV-aging induction, the laser group received a single fractional 1064 nm, 450 ps (subnanosecond) Nd:YAG treatment at 3.8 J/cm and 10 Hz using a 6 × 6 mm spot, with a measured pulse energy of 1.07 J and a calculated irradiance of 8.44 GW/cm; 30 stacks, corresponding to 30 laser shots delivered to the same target area, were applied over 3 s. UV exposure increased cytosolic pLATS1/LATS1, cytosolic pYAP, and ELISA-detected IQGAP1-associated pYAP signals while reducing nuclear YAP; laser treatment partially reversed these changes. Concurrently, laser treatment decreased ELISA-detected IQGAP1-associated pNFAT1 signals, restored nuclear NFAT1 localization, and reduced cytosolic pNFAT1. Quantitative immunofluorescence, histomorphometric, and ultrastructural analyses showed restoration of the collagen type I signal and collagen type I/III ratio and improvements in collagen density, coherency, angular deviation, and collagen bundle diameter. Laser treatment restored the expression of tendon/ligament-lineage markers, including scleraxis, mohawk homeobox, and tenomodulin; UV-induced elevations in osteogenic markers (RUNX2, SP7, and ALPL) were not significantly attenuated. Overall, fractional subnanosecond Nd:YAG laser treatment partially improved the matrix architecture of UV-aged rat facial retaining ligaments. These exploratory findings support an association model linking laser-associated matrix remodeling with coordinated changes in LATS1-YAP-IQGAP1-NFAT1 signaling, lineage-marker recovery, and collagen type I-dominant realignment, but do not establish a causal signaling sequence or functional mechanical strengthening. - Source: PubMed
Publication date: 2026/09/20
Oh SeyeonKim GeebumOh MyungjuneOh Seung MinKim Min SeungLee Jae IkSon Kuk HuiByun Kyunghee - Acute myeloid leukemia (AML) is a malignant tumor of the hematopoietic system. RhoA has been implicated in AML progression, but its role in regulating macrophage polarization and phagocytic function in the AML microenvironment remains unclear. - Source: PubMed
Publication date: 2026/09/25
Shen LiyunQiao Sha - The Hippo pathway and its downstream effectors Yes-associated protein/transcriptional coactivator with PDZ-binding motif-TEA domain transcription factor (YAP/TAZ-TEAD) play critical roles in organ-size control, tissue homeostasis, regeneration, and stem-cell biology. Their aberrant activation drives malignancies, fibrosis, cardiovascular disease, and immune dysregulation. Once regarded undruggable, the YAP/TAZ-TEAD complex has become one of the most actively pursued target classes in oncology and beyond. In this review, we delineate the biological functions of the Hippo-YAP/TAZ-TEAD axis and integrate its pathway physiology with the structural basis of druggability, centered on the Ω-loop surface pocket and the buried palmitoylation-binding pocket (PBP) of TEAD, whose distinct geometries dictate the pharmacophoric requirements, paralog selectivity, and resistance liabilities of current agents. We then systematically compare mechanism-guided therapeutic modalities, encompassing direct protein-protein interaction disruptors, covalent and noncovalent PBP inhibitors, proteolysis-targeting chimeras (PROTACs), and cofactor-interface modulators. We also analyze the upstream kinase (MST1/2, LATS1/2) modulators, direct YAP/TAZ inhibitors and degraders, and emerging gene-, RNA-, antibody-, and cell-based therapies. We critically evaluate preclinical and early clinical performance across oncology, fibrosis, immunology, and regenerative medicine, distinguishing robust proof-of-concept from clinically meaningful benefit. We further dissect resistance mechanisms, on-target safety concerns, and the therapeutic-window limitations of pan-TEAD inhibition. Ultimately, we outline rational combination strategies, biomarker-guided patient selection, and future directions for paralog-selective and tissue-restricted Hippo-targeted therapeutics. - Source: PubMed
Publication date: 2026/09/23
Qu XiaodanWang Zhan-You