ReviewCell death and differentiation2017
The LATS1 and LATS2 tumor suppressors: beyond the Hippo pathway.
Review in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
159 citing papers in PubMed, 1 synthesis or guideline pooled it, 265 citations in OpenAlex.
- Inflamed Yet Immune-Evasive? A Transcriptomic Meta-Analysis Identifies Conserved Inflammatory, Developmental, and Neuronal Signatures Associated with Polyploid Giant Cancer Cells.International journal of molecular sciences · 2026Pooled it
- Local control of Cre-regulated genetic modeling in vivo using wireless implantable optoelectronics.Science advances · 2026Article
- LATS1/2 inactivation drives a distinct venous endothelial cell response that contributes to fibrotic remodeling of the lung.Science advances · 2026Article
- Systematic analysis of hippo pathway signaling identifies TEAD1 as a transcriptional regulator of neuroendocrine prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- Genetic Medicine Approaches for Tumor Suppressor Loss: Therapeutic Replacement with Self-Amplifying RNA.Pharmaceutical research · 2026Review
- Enzymatic activity-independent NANS stabilizes LATS2 to drive growth and therapeutic resistance in HR+/HER2- breast cancer.Nature communications · 2026Article
- ITGB5 promotes immune escape in hepatocellular carcinoma by regulating PD-L1 through SETDB1/Hippo signaling pathway.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Targeting Sirtuins in Thyroid Cancer: Mechanisms, Drug Development, and Emerging Roles in Tumor Immunity and Ferroptosis.Cancers · 2026Review
- LATS1/2 Inhibitor Attenuates Osteoclast Differentiation via Hippo-YAP/TAZ Signaling Pathway and Alleviates Osteoporosis in Ovariectomized Rats.Current medical science · 2026Article
- Brain Metastases in Diffuse Pleural Mesothelioma: Clinical, Histologic, and Molecular Correlates.JTO clinical and research reports · 2026Article
- Quantifying rate-limiting genetic variation in breast and ovarian tumourigenesis.EBioMedicine · 2026Article
- A YAP/TAZ-CDC6 Axis Initiates and Maintains Malignant Transformation.Cancer science · 2026Article
- Subtype-Dependent Expression Patterns of Core Hippo Pathway Components in Thymic Epithelial Tumors (TETs): An RT-qPCR Study.Biomedicines · 2026Article
- Identification of cryptic KMT2A-PTD and other novel fusion genes by transcriptome sequencing alters molecular risk stratification in AML-NK.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Dose-dependent activation of the Hippo pathway by Type I and Type III interferons suppresses tissue repair by human bronchial epithelial cells.PLoS biology · 2026Article
- Article
- Lats1/2 Differentially Modulate the Proliferative State of Dental Epithelial Progenitors and Ameloblasts in the Murine Incisor.Orthodontics & craniofacial research · 2025Article
- METTL3-dependent m6A RNA methylation suppresses aberrant mammary epithelial differentiation and neoplastic transformation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeted degradation of endogenous YAP by nanobody bioPROTAC inhibits tumor progression.Nature communications · 2025Article
- Lats1/2 Are Essential for Developmental Vascular Remodeling and Biomechanical Adaptation to Shear Stress.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
99 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper cellular functionality and homeostasis are maintained by the convergent integration of various signaling cascades, which enable cells to respond to internal and external changes. The Dbf2-related kinases LATS1 and LATS2 (LATS) have emerged as central regulators of cell fate, by modulating the functions of numerous oncogenic or tumor suppressive effectors, including the canonical Hippo effectors YAP/TAZ, the Aurora mitotic kinase family, estrogen signaling and the tumor suppressive transcription factor p53. While the basic functions of the LATS kinase module are strongly conserved over evolution, the genomic duplication event leading to the emergence of two closely related kinases in higher organisms has increased the complexity of this signaling network. Here, we review the LATS1 and LATS2 intrinsic features as well as their reported cellular activities, emphasizing unique characteristics of each kinase. While differential activities between the two paralogous kinases have been reported, many converge to similar pathways and outcomes. Interestingly, the regulatory networks controlling the mRNA expression pattern of LATS1 and LATS2 differ strongly, and may contribute to the differences in protein binding partners of each kinase and in the subcellular locations in which each kinase exerts its functions.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.