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
- 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 CriagLorenzi 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 - The Hippo signaling pathway regulates cell proliferation, differentiation, and survival. LATS kinases (LATS1 and LATS2) are central kinases in this pathway, activated by MST/MAP4Ks through phosphorylation at the hydrophobic motif, which primes subsequent autophosphorylation at the activation loop. Here, we identify a conserved autophosphorylation site (Ser872 in LATS1 and Ser835 in LATS2) within a canonical HXRXXS motif of the kinase domain, designated as the canonical LATS1/2 substrate (CLS) site. Phosphorylation at the CLS site is required for full activation of LATS kinases, as substitution of this serine with alanine significantly impairs YAP phosphorylation, thereby enhancing YAP oncogenic activity, a key downstream effector of LATS kinases. These results provide new mechanistic insights into the regulation of LATS kinase activity and the biological function of the Hippo pathway. - Source: PubMed
Publication date: 2026/05/20
Jin RuxinZhong ZhenxingZhu RuiZhang AnlanLi JianYu Fa-XingWang Yu - To investigate the mechanism by which aerobic exercise improves transverse aortic constriction (TAC)-induced heart failure in mice. - Source: PubMed
Zhang GuodongWei SiangWang HongXie YanliHe HuiLi Rong - The extracellular matrix (ECM) defines the biomechanical and biochemical microenvironment of tissues, directing cell behaviour and phenotype. In the ovary, ECM must dynamically remodel in each cycle under hormonal regulation to control follicle development and produce fertilizable oocytes. Dysregulation of this process may result in aberrant formation of ECM as seen in polycystic ovary syndrome (PCOS) whose pathology includes fibrosis of the ovary and which is a major cause of infertility. PCOS is characterised by hyperandrogenism and, here, we investigate the impact of androgens on fibrosis, cell-ECM interactions and mechanosensing. We report an altered network of gene expression related to the genesis of fibrosis. Preantral follicles from C57BL/6 mice (14-15 days postpartum) were stimulated with dihydrotestosterone (DHT, 10nM) in 24/72 hours culture. Expression of fibrosis-associated genes (Eln; Ctgf; Acta2; Plod2; Hpse) significantly increased with androgen (72 h), as did TGF-β signalling (Tgfb1; Tgfb3). We show a direct connection between androgen and mechanosensing within the ovary, with androgen upregulating the mechanosensitive Hippo pathway (Yap1; Lats1; Lats2; Stk3; Stk4; Frmd6) and downstream targets (Ctgf; Axl; Cyr61). Our results highlight hyperandrogenism as a probable driver of the fibrosis in the polycystic ovary, and emphasise the importance of ECM regulation in follicle development and fertility. - Source: PubMed
Publication date: 2026/02/18
Hopkins Thomas I RLerner AvigdorDunlop Iain EFranks StephenHardy Kate