ライフサイエンスコーパス: LATS

1 Saccharomyces cerevisiae Cbk1 is a LATS/Ndr protein kinase and a downstream component of th

2 Saccharomyces cerevisiae Cbk1 kinase is a LATS/NDR tumor suppressor orthologue and component of th

3 ith a JNK-dependent increase in binding of a LATS inhibitor, LIMD1, to the LATS1 kinase and that redu

4 n alpha3 in TA cells that signals through an LATS-independent FAK/CDC42/PP1A cascade to control YAP-S

5 extent with WW45, KIBRA, and Angiomotin, and LATS co-migrated exclusively with USP9X during gel filtr

6 chanism independent of the kinases Hippo and LATS via which YAP is controlled by the innate immune pa

7 plained by the interaction of LIM-kinase and LATS.

8 he core of the pathway consists of a MST and LATS family kinase cascade that ultimately phosphorylate

9 , although serving as an adaptor for MST and LATS, Salvador can also bind RASSF1A.

10 together, the phosphorylation of Amot130 by LATS is found to be a key feature that enables it to inh

11 a substrate for the Saccharomyces cerevisiae LATS/NDR orthologue Cbk1, which controls polarized growt

12 The core LATS kinases of the Hippo tumor suppressor pathway phosp

13 atures, which are concomitant with decreased LATS and YAP phosphorylation, but not MST1/2.

14 significantly downregulated and destabilized LATS and resulted in enhanced nuclear translocation of Y

15 P binding to the Warts and Salvador homologs LATS and WW45.

16 n this study, we introduced human LATS1 into LATS(-/-) MEF cells by adenovirus-mediated gene transfer

17 -repression between the Hippo pathway kinase LATS/Warts (Wts) and growth regulator Melted generates m

18 The kinase LATS/WARTS is a tumor suppressor protein conserved in ev

19 tion of the large tumour suppressor kinases (LATS) 1 and 2, which are part of the Hippo pathway, prom

20 tly, the Amot130 (S175A) mutant, which lacks LATS phosphorylation, bound AIP4 poorly under all condit

21 mammalian orthologs, like salvador, merlin, LATS, and YAP1, have been implicated in tumorigenesis.

22 growth and homeostasis through a central MST-LATS kinase cascade.

23 RASSF1A-p.133Ser failed to activate the MST2/LATS pathway, which is required for YAP/p73-mediated apo

24 1-Mob2, to our knowledge the first of an NDR/LATS kinase-Mob complex.

25 hich is activated by the kinase Cbk1, an Ndr/LATS-related protein that functions in a system related

26 The Ndr/LATS family kinase Cbk1, functioning in a system similar

27 ivity is differentially regulated by the Ndr/LATS family kinase, Cbk1: phosphorylation suppresses PB/

28 ell proliferation and morphogenesis; the NDR/LATS family protein kinases, which associate with "Mob"

29 activation region that may be unique to NDR/LATS kinases, in which a key regulatory motif apparently

30 ynthase kinase 3 but not casein kinase 1 nor LATS in YAP-mediated TAZ loss.

31 rosine residue, which is critical for normal LATS function in vivo.

32 Absence of LATS stabilized ERalpha and the Hippo effectors YAP and

33 ts resulted in significant downregulation of LATS.

34 cal (that is, YAP/TAZ-independent) effect of LATS in the regulation of human breast cell fate.

35 athway by influencing the phosphorylation of LATS and YAP, but functional consequences of these bioch

36 In the presence of LATS, ERalpha was targeted for ubiquitination and Ddb1-c

37 kinases in MST1/2-independent regulation of LATS and YAP.

38 ns two WW domains and binds to the Warts (or LATS) protein kinase.

39 Finally, we show that dCSK phosphorylates LATS in vitro at a conserved C-terminal tyrosine residue

40 lts strongly indicate that USP9X potentiates LATS kinase to suppress tumor growth.

41 overexpression in murine podocytes promoted LATS kinase phosphorylation, leading to subsequent YAP S

42 -threonine kinase, a component of the RASSF1-LATS tumor suppressor network, is involved in cell proli

43 ed upon silencing of large tumor suppressor (LATS)-1 and LATS2, direct substrates of Mst2.

44 Large tumor suppressor (LATS)1/2 protein kinases transmit Hippo signaling in res

45 Furthermore, we find that LATS can synergize with F-actin perturbations by phospho

46 These biochemical observations indicate that LATS is a novel negative regulator of CDC2/cyclin A, a f

47 Here, we show that LATS proteins (mammalian orthologs of Warts) interact di

48 The LATS family of serine/threonine kinases control tissue s

49 d show that HSP90 inhibitors can disrupt the LATS tumor suppressor pathway in human cancer cells.

50 f LATS1 and decreased phosphorylation of the LATS substrate YAP, an oncoprotein transcriptional coact

51 Ssd1 is a substrate of the LATS/NDR tumour suppressor orthologue Cbk1 kinase.

52 r adaptor protein couples MST kinases to the LATS kinases to form the hippo pathway.

53 Thus, this LATS-mediated feedback loop provides an efficient mechan

54 lso shown that LATS2 kinase activity and two LATS conserved domains (LCDs) are required for Lats2 to

55 uman Ndr; and Drosophila and mammalian WARTS/LATS kinases.

56 ng a cytosolic Hippo kinase complex in which LATS kinase is inhibited.

57 cells, Ajuba LIM proteins/dJub interact with LATS/Warts (Wts) and WW45/Sav to inhibit phosphorylation

58 apen homolog MAP4K4 similarly interacts with LATS (Warts homolog) and promotes inhibition of YAP (Yor

59 rotein expression correlated positively with LATS but negatively with YAP/TAZ in pancreatic cancer ti

60 USP9X interacted strongly with LATS kinase and to a lesser extent with WW45, KIBRA, and