ライフサイエンスコーパス: invadopodium

1 bilization, and maturation into a functional invadopodium.

2 nd regulates PI(3,4)P2 levels locally at the invadopodium.

3 have lower invasive properties and impaired invadopodium activity.

4 We have dissected the stages of invadopodium assembly and maturation and show that invad

5 The mechanisms regulating invadopodium assembly and maturation are not understood.

6 oma cells and define four distinct stages of invadopodium assembly and maturation consisting of invad

7 th N-WASP and cortactin and is essential for invadopodium assembly, whereas WICH/WIRE regulates N-WAS

8 ocking the function of these SNAREs perturbs invadopodium-based ECM degradation and cell invasion.

9 tion mediates the recruitment of NHE1 to the invadopodium compartment, where it locally increases the

10 a 5'-inositol phosphatase, localizes at the invadopodium core and regulates PI(3,4)P2 levels locally

11 dia restricts cofilin activity to within the invadopodium core, resulting in a focused invadopodial p

12 ion of the Stx4 N-terminal peptide decreased invadopodium formation and cell invasion in vitro Of not

13 w that Munc18c is required for Stx4-mediated invadopodium formation and cell invasion.

14 ndings identify Pyk2 as a unique mediator of invadopodium formation and function and also provide a n

15 terestingly, we show that macrophage-induced invadopodium formation and tumor cell intravasation also

16 tand how the tumor microenvironment controls invadopodium formation and tumor cell locomotion, we sys

17 During invadopodium formation in MDA-MB-231 human breast cancer

18 We have studied the molecular mechanisms of invadopodium formation in metastatic carcinoma cells.

19 tor (EGF) receptor kinase inhibitors blocked invadopodium formation in the presence of serum, and EGF

20 signaling pathway blocked macrophage-induced invadopodium formation in vitro and the dissemination of

21 dicate that EGF receptor signaling regulates invadopodium formation through the N-WASP-Arp2/3 pathway

22 Surprisingly, RalB-mediated invadopodium formation was dependent on RalBP1/RLIP76 bu

23 The increased invadopodium formation was directly dependent on EGFR si

24 Invadopodium formation was enhanced by the expression of

25 Invadopodium formation was not dependent on the canonica

26 Munc18c and Stx4, which was enhanced during invadopodium formation, and that a reduction in Munc18c

27 Tks5 regulates invadopodium formation, but the precise timing during in

28 of fascin and other TGFbeta response genes, invadopodium formation, cell migration, and invasion, su

29 s revealed that expression of HBEGF enhanced invadopodium formation, thus providing a mechanism for c

30 F receptor (EGFR) to the cell surface during invadopodium formation.

31 ated biochemical and signaling mechanism for invadopodium formation.

32 on of the ATPase function of RalBP1 impaired invadopodium formation.

33 d K-Ras is both necessary and sufficient for invadopodium formation.

34 a reduction in Munc18c expression decreases invadopodium formation.

35 F stimulation of serum-starved cells induced invadopodium formation.

36 ors, Nck1, Cdc42, and WIP, are necessary for invadopodium formation.

37 receptor and Src tyrosine kinases to promote invadopodium function in breast cancer cells, thereby pr

38 ively active Rac3 can rescue the deficits in invadopodium function in Vav2-knockdown cells.

39 HBEGF expression also resulted in enhanced invadopodium function via upregulation of matrix metallo

40 ub for signaling molecule recruitment during invadopodium generation and cancer progression, as well

41 Herein, we show that the macrophage-induced invadopodium is formed through a Notch1/Mena(INV) signal

42 se PTP1B, and that PTP1B localization to the invadopodium is reduced by Mena(INV) expression.

43 ium formation, but the precise timing during invadopodium lifetime (initiation, stabilization, matura

44 that Vav2 function is required for promoting invadopodium maturation and consequent actin polymerizat

45 /WIRE regulates N-WASP activation to control invadopodium maturation and degradative activity.

46 cortactin is a master switch that activates invadopodium maturation and function.

47 ascade is known to be a critical trigger for invadopodium maturation and subsequent cell invasion in

48 We conclude that Mena(INV) promotes invadopodium maturation by inhibiting normal dephosphory

49 f Arg, arguing that Src indirectly regulates invadopodium maturation through Arg activation.

50 w that forced Mena(INV) expression increases invadopodium maturation to a far greater extent than equ

51 interaction with WIP and WICH/WIRE modulates invadopodium maturation; changes in WIP and WICH/WIRE le

52 regulates tumor cell invasion by controlling invadopodium-mediated functions, FAK controls invasivene

53 sin family proteins and is known to regulate invadopodium-mediated matrix degradation.

54 When an invadopodium penetrates basement membrane, it rapidly tr

55 solution spatiotemporal live-cell imaging of invadopodium precursor assembly.

56 The timing of SHIP2 arrival at the invadopodium precursor coincides with the onset of PI(3,

57 -dimensional matrices but is dispensable for invadopodium precursor formation in metastatic human bre

58 podium assembly and maturation consisting of invadopodium precursor formation, actin polymerization,

59 nsights into molecular mechanisms underlying invadopodium precursor initiation, stabilization, and ma

60 beta1 integrin is activated during invadopodium precursor maturation, and forced beta1 inte

61 filin, and actin arrive together to form the invadopodium precursor, followed by Tks5 recruitment.

62 Mena(INV) is recruited to invadopodium precursors just after their initial assembl

63 Phosphorylation of the invadopodium protein cortactin is a master switch that a

64 n activation regulates the dynamic cycles of invadopodium protrusion and retraction and is essential

65 nments, finding that only tumor cells in the invadopodium-rich microenvironments degraded extracellul

66 nt actin polymerization, leading to impaired invadopodium stability and matrix degradation.