LATS1 / LATS2 pThr1079/1041 antibody Ab
- Known as:
- LATS1 / LATS2 pThr1079/1041 (anti-) Antibody
- Catalog number:
- 1488143
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- LATS1 / LATS2 pThr1079/1041 antibody
Related genes to: LATS1 / LATS2 pThr1079/1041 antibody Ab
- 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
- Gene:
- LATS2 NIH gene
- Name:
- large tumor suppressor kinase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 13q12.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-07
- Date modifiied:
- 2015-09-03
Related products to: LATS1 / LATS2 pThr1079/1041 antibody Ab
Related articles to: LATS1 / LATS2 pThr1079/1041 antibody Ab
- Endothelial dysfunction is recognized to contribute to chronic tissue remodeling in the lung, yet endothelial-derived mechanisms driving these processes remain largely undefined. Here, we show that endothelial inactivation of the LATS1 and LATS2 kinases, key suppressors of the transcriptional regulators YAP and TAZ, elicits distinct responses depending on endothelial identity within different pulmonary vascular beds. Our data indicate that LATS1/2 inactivation in general capillary endothelial cells induces a reactive capillary injury-like state, whereas a separate endothelial population located within veins adopts a distinct profibrotic state. We show that expansion of this reactive venous endothelial cell population, which is marked by EBF1 and ACKR1 expression, is associated with fibroblast activation, macrophage accumulation, and epithelial remodeling, collectively generating a microenvironment characteristic of fibrotic lung disease. We further demonstrate that pharmacologic inhibition of YAP/TAZ-TEAD signaling prevents stromal and immune remodeling and fibrotic lesion formation following endothelial LATS1/2 inactivation. These findings identify LATS1/2-mediated restraint of YAP/TAZ as essential for lung endothelial homeostasis and highlight a distinct venous cell response as a direct contributor to fibrotic lung remodeling. - Source: PubMed
Publication date: 2026/08/28
Kontodimas KonstantinosRaslan Ahmed ASpira BenjaminZhu CrystalKarapurkar JanardhanKefella YohanaChiu DarrenQiu XintaoBeane Jennifer ELigresti GiovanniVarelas Xaralabos - This study reports the generation and comprehensive characterization of the LATS1/2 knockdown (KD) induced pluripotent stem cell (iPSC) line, MUSIi012-A-9. Created via CRISPR/Cas9-mediated modification of the LATS2 gene in a parental LATS1-KD line, this resource serves as a crucial human model to investigate the roles of LATS1/2 kinases, key regulators of the Hippo signaling pathway. Comprehensive validation confirmed normal iPSC morphology, pluripotency marker expression (OCT3/4, NANOG, SOX2), genetic stability (46,XX karyotype), and robust multilineage differentiation potential. This well-characterized iPSC line is a vital tool for advancing research into Hippo pathway regulation, lineage specification, and cell fate determination in development and disease. - Source: PubMed
Publication date: 2026/06/29
Lorthongpanich ChanchaoSrisook PimonwanJiamvoraphong NittayaKlaihmon PhatchanatKumsui SirilukLaowtammathron ChutiIssaragrisil Surapol - Research focused on studying Hippo signaling up- and downregulation in a model of mouse lung cell regeneration. The cell-specific role of the activation and inhibition of Hippo signaling is demonstrated at the cellular level within the context of a unified bronchoalveolar lung organoid model. We used pharmacological modulators of Hippo pathway components-TRULI and verteporfin. The findings revealed that inhibition of Lats1/2 kinases via TRULI leads to different levels of Hippo gene expression for different lung cell types. The inhibition of Lats1/2 kinases enhances cell proliferation in the bronchiolar epithelium, while verteporfin suppresses it. However, no changes in the cellular composition of the bronchiolar epithelium (except ciliated cells) were observed with either TRULI or verteporfin. Inhibition of Lats1/2 kinases in the alveolar epithelium leads to a decrease in type 2 alveolocytes and alters their differentiation trajectories. The results demonstrate a cell-specific influence of Hippo modulation on the lung cells and may prove useful for the development of novel therapeutic approaches for the treatment of respiratory pathologies. - Source: PubMed
Publication date: 2026/06/19
Govorova Irina ANovikova Yulia ASutyagina Oksana INikitochkina Sofya YSabirov Marat SStarinnov Zahar RVolozhinskaia Alexandra AVorotelyak Ekaterina A - Treatment-induced neuroendocrine prostate cancer (NEPC) represents an aggressive form of castration-resistant prostate cancer (CRPC) associated with lineage plasticity and therapeutic resistance. In this study, we investigated the role of the Hippo signaling axis in the transdifferentiation from androgen receptor-positive prostate cancer (ARPC) to NEPC. RNA sequencing analyses of CRPC metastases revealed coordinated alterations in Hippo pathway components, with decreased expression of YAP1, LATS2, and TEAD2 and increased expression of LATS1, TEAD1, and the RNA splicing regulator RBFOX2 in NEPC. These transcriptional alterations were consistently observed across multiple model systems and patient samples. Epigenetic analyses demonstrated that reduced expression of YAP1, TEAD2, and LATS2 was associated with increased DNA methylation, whereas elevated TEAD1 expression correlated with DNA hypomethylation in NEPC. NEPC selectively retained TEAD1 expression, including a spliced isoform not detected in ARPC. Proteomic interactome analyses revealed that TEAD1 associated with RNA splicing factors and DNA repair proteins. Functional studies showed that TEAD1 knockdown led to the reversion of gene programs associated with epithelial differentiation. These findings indicate that the conversion of ARPC to NEPC involves coordinated loss of AR, YAP1, and REST activity alongside sustained TEAD1 expression and altered RNA processing. Our data identify TEAD1 as a transcriptional regulator associated with the NEPC state and suggest a role for TEAD1-linked transcriptional and post-transcriptional mechanisms in prostate cancer lineage plasticity. - Source: PubMed
Publication date: 2026/05/30
Brown Lisha GColeman Ilsa MChu Tony L HSayar ErolcanPatel Radhika AHanratty BrianAdil MohamedLi DapeiLi YongtaoNguyen Holly MSessions Conner JSweeney Erin LAlumkal Joshi Jda Costa Rui M GilWang YuzhuoLin Daniel WTrue Lawrence DDumpit RuthCorey EvaLee John KNelson Peter SXin LiHaffner Michael CMorrissey Colm - Atherothrombosis, which underlies most acute coronary syndromes and is driven by intraplaque thrombosis, preferentially occurs in regions of disturbed blood flow (d-flow). Although LATS1/2 (large tumor suppressor kinases 1 and 2) are known regulators of endothelial mechanotransduction, the mechanisms by which d-flow connects endothelial senescence, proliferation, and intraplaque thrombosis remain poorly understood. - Source: PubMed
Publication date: 2026/05/27
Kotla SivareddyLee JonghaeKo Kyung AeChen WeiqingSamanthapudi Venkata Subrahmanya KumarHoang OanhMejia Gilbert FLi ShengyuLee HaniZhang AijunCho Min SoonSchadler Keri LRivera Luis AntonioImanishi MasakiTavares Samperio Kay CarleneKim Jung HyunOstos-Mendoza Kelia CMariscal-Reyes Karla NDeswal AnitaCooke John PFujiwara KeigiPalaskas Nicolas LKoutroumpakis EfstratiosGi Young JinPathania RajneeshMorrell CraigLorenzi Philip LTan LinMahmud IqbalHanssen Nordin M JAfshar-Kharghan VahidHamilton Dale JYvan-Charvet LaurentChini Eduardo NHerrmann JoergVasquez Hernan GShen Ying HMartin James FXu HaodongSeeley Erin HBurks Jared KBrookes Paul SWang GuangyuLe Nhat-TuAbe Jun-Ichi