ライフサイエンスコーパス: mitogenesis

1 functions, including vesicle trafficking and mitogenesis.

2 rgize to promote PCC invasion, survival, and mitogenesis.

3 e, and the down-regulation of GATA-6 induces mitogenesis.

4 palmitoylated SFK and promote EGF-dependent mitogenesis.

5 wide range of cellular functions, including mitogenesis.

6 in T and AT are involved in cell growth and mitogenesis.

7 mouse Grb10 (mGrb10alpha) on IGF-I-mediated mitogenesis.

8 at RUL may function as a common regulator of mitogenesis.

9 n beta-cells, contributing to an increase in mitogenesis.

10 sion was 15-fold greater and PACAP inhibited mitogenesis.

11 alter fibroblast growth factor 2 actions on mitogenesis.

12 chanism of small-t-antigen action to promote mitogenesis.

13 n, IGF-I failed to significantly affect cell mitogenesis.

14 to NIH3T3 fibroblasts inhibited PDGF-induced mitogenesis.

15 ng pathways, which results in an increase in mitogenesis.

16 ls of stimulation of IGF-I- and PDGF-induced mitogenesis.

17 iferation but was required for IGF-1-induced mitogenesis.

18 t EPO-R Tyr-343 is important in EPO-mediated mitogenesis.

19 30 nm or less, but only modest inhibition of mitogenesis.

20 ment to glucose-induced pancreatic beta-cell mitogenesis.

21 vation, cell migration, and endothelial cell mitogenesis.

22 d regulatory loop plays a key role in T cell mitogenesis.

23 the IGF-IR and fail to respond to IGF-I with mitogenesis.

24 tic basis for the serum dependence of T cell mitogenesis.

25 nsulin-like growth factor I (IGF-I)-mediated mitogenesis.

26 determined to be essential for Rac1-mediated mitogenesis.

27 ine the potential role of these receptors in mitogenesis.

28 n of IGF-I and IL-4 that sustains the intact mitogenesis.

29 nce of the Shc/MAPK pathway in IGF-I-induced mitogenesis.

30 e of binding to FGFR1 enhanced FGF-2-induced mitogenesis.

31 onin receptor subtype capable of stimulating mitogenesis.

32 the former inducing apoptosis and the later mitogenesis.

33 part this might explain reported effects on mitogenesis.

34 on VSMCs to potentiate growth-factor-induced mitogenesis.

35 h DA-stimulated tyrosine phosphorylation and mitogenesis.

36 uptake in PASMC, indicating a role in PASMC mitogenesis.

37 has been shown to down-regulate LPA-mediated mitogenesis.

38 /hematopoietic modulation, angiogenesis, and mitogenesis.

39 ved at the Edg receptors is not reflected in mitogenesis.

40 global cytoskeleton remodeling accompanying mitogenesis.

41 cell migration and shape change rather than mitogenesis.

42 sary for ROI generation and thrombin-induced mitogenesis.

43 generation is necessary for thrombin-induced mitogenesis.

44 1 (ICAM) on B-lymphoid Raji cells results in mitogenesis.

45 growth-promoting proteins are necessary for mitogenesis.

46 cellular signal-regulated kinase), prevented mitogenesis.

47 ffness is altered in the range that controls mitogenesis.

48 contrast, STAT5 is not required for brain EC mitogenesis.

49 lation of negative regulators contributes to mitogenesis.

50 n the process of cAMP stimulation of thyroid mitogenesis.

51 ired cofactor for binding and hence cellular mitogenesis.

52 tic signals for cell function, in particular mitogenesis.

53 ts synergistically with PKA in cAMP-mediated mitogenesis.

54 hase-promoting complex, which increases cell mitogenesis.

55 RK1/2 pathways contribute to PI3-K-dependent mitogenesis.

56 C zeta (PKC zeta) to suppress Akt-dependent mitogenesis.

57 dins of relevance to pain, inflammation, and mitogenesis.

58 dogenous SNAT1 substrate required for T cell mitogenesis.

59 nown to initiate VSMC de-differentiation and mitogenesis.

60 GF-I-dependent Shc phorylation, and impaired mitogenesis.

61 ction was also required for IGF-I-stimulated mitogenesis.

62 hways contribute to its inhibitory effect on mitogenesis.

63 omotes sustained kinase activity critical to mitogenesis.

64 selectively cooperates with uPAR to mediate mitogenesis.

65 ly through the A1 receptor, leading to CASMC mitogenesis.

66 s a negative regulator of insulin-stimulated mitogenesis.

67 ffect in vitro glioma cell growth nor T cell mitogenesis.

68 orporation was used to evaluate EGF-in-duced mitogenesis.

69 r levels leading to a reduced IGF-I-mediated mitogenesis.

70 stal-induced metalloproteinase synthesis and mitogenesis; (4) crystal upregulation of matrix metallop

71 d no effect on either basal or EGFR-mediated mitogenesis (96 +/- 15% at 50 ng/ml).

72 vating factor; by contrast, endothelial cell mitogenesis, a repair process important to tissue surviv

73 ibited receptor tyrosine phosphorylation and mitogenesis after stimulation of cells by appropriate li

74 e, suggesting that PDGFRalpha contributes to mitogenesis and actin reorganization through diverse dow

75 epatic progenitor cells secondary to delayed mitogenesis and activated Wnt signaling.

76 concentration-dependent fashion and promotes mitogenesis and anchorage-dependent cloning.

77 A fuller understanding of how ROS regulate mitogenesis and apoptosis in vascular smooth muscle and

78 cellular signalings and processes including mitogenesis and calcium entry.

79 scades and its function is critical for both mitogenesis and carcinogenesis.

80 lity with insulin/IGF-I signaling to promote mitogenesis and cell growth.

81 ) plays a crucial role in alpha(2)M*-induced mitogenesis and cell proliferation.

82 al melanoma cells, we assessed the degree of mitogenesis and cell survival by bromodeoxyuridine incor

83 We show that Gas6 mediates mitogenesis and cell survival in Mel 290 cells.

84 PLC-IP(3) pathway and its ability to promote mitogenesis and cellular proliferation is not clear.

85 sts and GM7373 endothelial cells, as well as mitogenesis and chemotaxis of NIH-3T3 cells.

86 P) is a bioactive sphingolipid implicated in mitogenesis and cytoskeletal remodelling.

87 Mitogenesis and cytotoxicity of human periodontal ligame

88 inactive analog of APC), stimulates neuronal mitogenesis and differentiation from fetal human neural

89 henotype of mesangial cells, with suppressed mitogenesis and downregulation of alpha-smooth muscle ac

90 lect EGF-like repeats of tenascin-C elicited mitogenesis and EGFR autophosphorylation in an EGFR-depe

91 nsformation or in spontaneous human cancers, mitogenesis and expression of urokinase (uPA) and its re

92 ll (MVIC) homeostasis through its effects on mitogenesis and extracellular matrix biosynthesis.

93 found that micromolar levels of DA stimulate mitogenesis and glial fibrillary acidic protein (GFAP) e

94 and plays important roles in cell survival, mitogenesis and invasion.

95 ory effect of Dok-1 on growth factor-induced mitogenesis and its role as a tumor suppressor.

96 tion with deregulation of smooth muscle cell mitogenesis and leakage of newly formed blood vessels.

97 his process by activating smooth muscle cell mitogenesis and leukocyte adhesion.

98 his process by activating smooth muscle cell mitogenesis and leukocyte adhesion.

99 n that influence or occur as a result of SEC mitogenesis and migration during regeneration of the liv

100 FR-1, which is required for thrombin-induced mitogenesis and migration.

101 rate independently leading to an increase in mitogenesis and MMP synthesis and ultimately complementi

102 dently, ultimately leading to an increase in mitogenesis and MMP synthesis, and may converge downstre

103 that mediate distinct HGF responses such as mitogenesis and motility is regulated by HS-c-Met intera

104 hat Src activation is required for human ASM mitogenesis and motility.

105 IGF-II stimulates both mitogenesis and myogenesis through its binding and activ

106 EGFR2 (KDR/Flk-1)] mediates endothelial cell mitogenesis and permeability increases, whereas the role

107 demonstrated a possible role for PKCalpha in mitogenesis and PKCbeta1/2 in wound recovery.

108 ypes, while Ad2/PDGF-1308 potently inhibited mitogenesis and proliferation.

109 EET synthesis in EGF-mediated signaling and mitogenesis and provide compelling evidence for the PLA2

110 Significantly promoted mitogenesis and reduced cytotoxicity of hPDLCs were note

111 ll atrophy that was characterized by delayed mitogenesis and reduced glycolytic flux.

112 ulin axis participates in 5-HT-induced PASMC mitogenesis and RhoA/ROCK signaling, and may be an inter

113 omologue of PDGF-BB, as well as PDGF-induced mitogenesis and signaling by preventing phosphorylation

114 yc, that is important in normal PDGF-induced mitogenesis and subverted in Src transformation.

115 er of the novel PKC family, has key roles in mitogenesis and survival in normal and cancer cells.

116 and its ligands from promoting keratinocyte mitogenesis and survival to mediating FasL-induced epide

117 been reported to reduce pancreatic beta-cell mitogenesis and to increase apoptosis.

118 The ability of the IGF-IR to induce mitogenesis and to promote survival of cells against a v

119 which STAT-signaling pathways contribute to mitogenesis and transformation are not fully defined.

120 cular endothelial growth factor and to limit mitogenesis and tube formation.

121 crovascular endothelial cell-1 (HMEC-1) cell mitogenesis and tubular morphogenesis in three-dimension

122 imuli lead to the constitutive activation of mitogenesis and uPA and its receptor expression, through

123 y intermediates responsible for induction of mitogenesis and wound recovery.

124 function is required for 5-HT-induced PASMC mitogenesis, and 5-HT activates RhoA; however, the signa

125 logical processes such as membrane ruffling, mitogenesis, and chemotaxis.

126 ading to changes in cell shape and motility, mitogenesis, and development.

127 , migration, survival, growth factor-induced mitogenesis, and endothelial tubule formation are all me

128 ons including metabolic pathways, apoptosis, mitogenesis, and membrane trafficking.

129 mitogen-activated protein kinase activation, mitogenesis, and motogenesis, demonstrating that structu

130 nt for BRK's ability to enhance mammary cell mitogenesis, and raises the possibility that breast tumo

131 uction pathways involved in hormone release, mitogenesis, and tumor promotion.

132 neuropathology in vivo, suppression of brain mitogenesis, and ultimately neurogenesis, may provide a

133 2 membrane translocation, ERK1/2 activation, mitogenesis, and wound recovery, suggesting a mechanism

134 which these growth factors mediate beta-cell mitogenesis; and 3) whether activation of this/these sig

135 a cation current and probably contributes to mitogenesis; and stimulate release of Ca(2+) from intrac

136 report, VEGF-Ax stimulates endothelial cell mitogenesis, angiogenesis, as well as vascular permeabil

137 ase (PI3K) inhibitors diminished HGF-induced mitogenesis, anti-apoptosis, and MAP kinase activation,

138 ted kinase (ERK)-2 pathway to participate in mitogenesis, apoptosis, and cytokine production.

139 In contrast, PDGF-BB-mediated mitogenesis appears to depend on the SH2 but not on the

140 ed half-life of intact 2D1 provides enhanced mitogenesis as compared with IL-2.

141 but for inhibition of cell proliferation and mitogenesis as well.

142 activation was required for maximal PC3 cell mitogenesis, as measured by 5-bromo-2'-deoxy-uridine inc

143 tokines are known regulators of keratinocyte mitogenesis, as well as lipid synthesis in extracutaneou

144 r were antagonists, in quinpirole-stimulated mitogenesis at hD3 receptors, several of the hydroxybuty

145 s ligand inhibited quinpirole stimulation of mitogenesis at human dopamine D3 receptors transfected i

146 This study completes the mitogenesis-based comparison of receptor specificity of

147 d IGF-I and lysophosphatidic acid-stimulated mitogenesis but had no effect on epidermal growth factor

148 t bind p110, had no effect on EGF-stimulated mitogenesis but still blocked EGF-stimulated lamellipod

149 regation response is consistent with that of mitogenesis, but not with Edg-2, -4, and -7.

150 eceptor system generates opposing effects on mitogenesis by differentially regulating signaling pathw

151 The repression of serum-induced mitogenesis by differentiation correlates with repressio

152 cle cells, GATA-6 has been shown to regulate mitogenesis by driving cells into a quiescent state, and

153 target Merlin, suggesting that PAK promotes mitogenesis by phosphorylating, and thus inactivating, M

154 chanism of bombesin-dependent stimulation of mitogenesis by regulating directly the cell cycle in pro

155 mally demonstrate that Hh signaling promotes mitogenesis by suppression of p16.

156 the regulation of uterine smooth muscle cell mitogenesis by the glycosaminoglycan heparin, which has

157 nctions, including vascular permeability and mitogenesis, by activating their cognate receptors, brad

158 Our evidence shows that differentiation and mitogenesis can both occur independently of pre-TCR expr

159 Pertussis toxin and PD 98059 blocked the mitogenesis caused by bromocriptine, suggesting a role f

160 sis in H4IIE cells or hepatocytes, increased mitogenesis caused by direct Gialpha-protein stimulation

161 th tyrosine kinase activity that can mediate mitogenesis, cell transformation, and inhibition of apop

162 hway may contribute to the enhanced cellular mitogenesis characteristic of hepatocellular carcinoma (

163 significant HGF-SF stimulation of total cell mitogenesis dependent on both IGF-I and HGF-SF dose (194

164 a positive as well as an inhibitory role in mitogenesis depending on the cell context has been impli

165 ediated activation of Rap1 and cAMP-mediated mitogenesis depends on the subcellular localization of E

166 al cells and sensitized them to FGF2-induced mitogenesis despite the fact that glypican-1 remained a

167 on of VEGFR-2 expression appears critical in mitogenesis, differentiation, and angiogenesis.

168 hatidylinositol (3,4,5)-triphosphate-induced mitogenesis during human cancer pathogenesis.

169 PI3K signaling pathways is insufficient for mitogenesis elicited through c-Met.

170 ell migration (phospholipase-C gamma) and/or mitogenesis (extracellular signal/regulated-mitogen-acti

171 cellular functions, including proliferation, mitogenesis, formation of branching tubules, angiogenesi

172 ed to be D2R/D3R agonists in both GoBRET and mitogenesis functional assays.

173 s surprisingly positive effects on beta-cell mitogenesis, glucose sensing, beta-cell markers of diffe

174 ver, how Dok-1 exerts its negative effect on mitogenesis has remained elusive.

175 tive Stat3beta protein inhibits PDGF-induced mitogenesis in a manner that is reversed by ectopic c-My

176 has been shown to promote cell adhesion and mitogenesis in both fibroblasts and endothelial cells an

177 14,15-EET failed to induce mitogenesis in cell lines expressing minimal HB-EGF, whe

178 The ability of S1P to induce mitogenesis in cells expressing the EDG-1 subfamily of G

179 re known to be sufficient for IGF-I-mediated mitogenesis in cells overexpressing the IGF-IR, the mito

180 growth factor pleiotrophin (PTN) can induce mitogenesis in cells that express the receptor for this

181 last growth factor promotes angiogenesis and mitogenesis in colon carcinomas.

182 tment of Rac to matrix adhesions and promote mitogenesis in confluent cells.

183 tal HCA-7 cell conditioned medium stimulated mitogenesis in COX-depleted HCA-7 cells and COX-null HCT

184 a demonstrate that ethanol enhances cellular mitogenesis in experimental HCC as a result of, at least

185 e ethanol had no significant effect on basal mitogenesis in H4IIE cells or hepatocytes, increased mit

186 n contrast, HGF significantly inhibited cell mitogenesis in HCC lines (68.4% +/- 9.4% vs. control, n

187 osa-6(Z) 15(Z)-dienoic acid (WIT003) induced mitogenesis in HUVECs and angiogenesis in the rat cornea

188 i-proteins using M7 failed to alter cellular mitogenesis in isolated cultured hepatocytes, whether in

189 neuregulin-1 (NRG-1) growth factors promote mitogenesis in MPNSTs, we examined the expression and ac

190 independent of PI3K to enhance HGF-dependent mitogenesis in myeloid cells, and possibly other common

191 is required for growth factor signaling and mitogenesis in nonimmune cells.

192 signaling and are required for PDGF-induced mitogenesis in normal cells.

193 suppressor merlin, thus removing a block to mitogenesis in normal cells.

194 sent study, we demonstrate that ET-dependent mitogenesis in rat neonatal and adult aortic smooth musc

195 s of EGFR blockade on pancreatic cancer cell mitogenesis in relation to activation of specific signal

196 hocyte function in vitro, including impaired mitogenesis in response to antigens of Mycobacterium lep

197 to determine which of these pathways control mitogenesis in response to physiologically relevant chan

198 ng that an AR autocrine loop is required for mitogenesis in SUM149 cells.

199 These involve the stimulation of mitogenesis in synovial fibroblasts and the secretion of

200 m, indicating that Wnt-1 protein can promote mitogenesis in the absence of an ER alpha-mediated respo

201 d allowed the receptor to promote Ba/F3 cell mitogenesis in the absence of EGF, arguing that these ar

202 First, by increasing mitogenesis in the absence of the p53 checkpoint in G2,

203 secreted protein that controls cell fate and mitogenesis in the developing nervous system.

204 able serum levels of MSeA on ECGS-stimulated mitogenesis in the mid- to late-G(1) phase, and the targ

205 IGFBP4 effectively inhibited IGF-stimulated mitogenesis in these cells.

206 t-derived growth factor-BB (PDGF-BB)-induced mitogenesis in vascular smooth muscle cells (VSMC).

207 protein-coupled receptor, has been linked to mitogenesis in vascular smooth muscle cells, but the mec

208 ous tuberculin responses, and reduced T cell mitogenesis in vitro, are well characterized.

209 To determine whether Rap1b stimulates mitogenesis in vivo, we have constructed a transgenic mo

210 sensitivity and decreases insulin-dependent mitogenesis in vivo.

211 via Stat1, inhibited EGF- or PDGF-stimulated mitogenesis in wild-type fibroblasts but enhanced [3H]th

212 f circulating T cells and compromised T-cell mitogenesis, increased viral burden in the bursae of IBD

213 udin inhibits thrombin-, but not FXa-induced mitogenesis, indicating that FXa acts independently of t

214 demonstrate that PKD selectively potentiates mitogenesis induced by bombesin or vasopressin in Swiss

215 verexpression of PKD selectively potentiates mitogenesis induced by bombesin, vasopressin, or PDBu in

216 Overexpression of iex-1 suppressed mitogenesis induced by platelet-derived growth factor (2

217 phate (S1P) mediates cellular proliferation, mitogenesis, inflammation, and angiogenesis.

218 -induced neurite regression was a prelude to mitogenesis initiated by a rise in intracellular calcium

219 and progression of prostate cancer, such as mitogenesis, invasiveness, angiogenesis, and metastasis.

220 Mitogenesis is dependent on lacritin's C-terminal domain

221 owth factor signal transduction pathways and mitogenesis is not well understood.

222 The TIMP-2 suppression of mitogenesis is reversed by the adenylate cyclase inhibit

223 Failure to activate caspase-8 during T cell mitogenesis leads to hyperactive autophagy and cellular

224 l mechanism of G(q)-coupled receptor-induced mitogenesis mediated by sustained PKD activation through

225 ted hepatocyte growth factor/c-Met-dependent mitogenesis, migration, cell scatter, and tubulogenesis.

226 wth factor (HGF/SF) receptor, Met, regulates mitogenesis, motility, and morphogenesis in a cell type-

227 saminoglycan-binding protein that stimulates mitogenesis, motogenesis, and morphogenesis in a wide ar

228 Hepatocyte growth factor (HGF) stimulates mitogenesis, motogenesis, and morphogenesis in a wide ra

229 Although insufficient for mitogenesis, mp110*ER enhanced Stat5-mediated proliferat

230 This mitogenesis occurs about 29 h after exposure to DA and r

231 eted NELL2 acts paracrinely to stimulate the mitogenesis of adjacent cells within the nascent DRG.

232 e therefore explored their role in mediating mitogenesis of airway smooth muscle.

233 esponsible for the adrenergic stimulation of mitogenesis of cardiac fibroblasts.

234 ts in the development of the DRG such as the mitogenesis of DRG progenitor cells and the differentiat

235 y for FGF2 and their ability to support FGF2 mitogenesis of heparan sulfate-deficient cells expressin

236 he receptor and to inhibit both VEGF-induced mitogenesis of human endothelial cells in vitro and tumo

237 vascular endothelial growth factor-dependent mitogenesis of human endothelial cells without inhibitin

238 han its parent antibodies to VEGF-stimulated mitogenesis of human endothelial cells, as well as both

239 reviously reported that IL-13 stimulated the mitogenesis of lung fibroblasts via platelet-derived gro

240 his study, we show that IL-13 stimulates the mitogenesis of mouse, rat, and human lung fibroblasts th

241 tudy tested the hypothesis that 5-HT induces mitogenesis of PASMC by down-regulating GATA-6.

242 nels with clotrimazole or TRAM-34 suppressed mitogenesis of preactivated lymphocytes, whereas resting

243 showed that IL-1beta enhanced IL-13-induced mitogenesis of rat lung fibroblasts through up-regulatio

244 p(22), margatoxin, and correolide suppressed mitogenesis of resting T-cells but not preactivated T-ce

245 on of developing granule cells and increased mitogenesis of the granule cell neuroblasts refractory t

246 a MAPK kinase inhibitor was able to suppress mitogenesis of the IGF-IR transfectants in response to I

247 articipation in 5-HT receptor 1B/1D-mediated mitogenesis of vascular SMCs through an effect on cytopl

248 tiple pathways contribute to cAMP-stimulated mitogenesis, only some of which are PKA dependent.

249 s, whereas SB203580 inhibited EGF-stimulated mitogenesis, p38 MAPK activation, and MAPK-activated pro

250 ceptor and down-regulates the Ras/MAP kinase mitogenesis pathway.

251 grins are required for activation of the ERK mitogenesis pathway.

252 In addition, MVIC mitogenesis per (3)H-thymidine ((3)HTdR) demonstrated a

253 icate IGF-I, PDGF-BB, and TGF-beta influence mitogenesis, phenotypic gene expression profile, and bio

254 s the effects of growth factors and serum on mitogenesis, proliferation, and cell cycle progression.

255 these pathways in acini have been linked to mitogenesis, protein synthesis, and regulation of the cy

256 rlecan, biglycan, and syndecans 1 and 3) and mitogenesis-related signaling proteins (e.g., mitogen-ac

257 ructs, it was determined that carcinoma cell mitogenesis required proteolytic shedding of syndecan-1

258 The mitogenesis requires a D2-receptor-mediated protein tyro

259 hance basic fibroblast growth factor-induced mitogenesis similar to wild type.

260 ine kinase associated receptors to stimulate mitogenesis, so MT can be considered as a permanently ac

261 GH)-induced membrane ruffling, and increases mitogenesis stimulated by platelet-derived growth factor

262 n dissected to reveal: 1) that Epo-dependent mitogenesis, survival, and bcl-x gene expression via ER-

263 ion rates, indicating roles for calpain 2 in mitogenesis, survival, and motogenesis.

264 lopment and maintenance including effects on mitogenesis, survival, fate determination, differentiati

265 are more effective in suppressing lymphocyte mitogenesis than either compound alone.

266 notype, such as the RAS pathway (involved in mitogenesis), the PI3K pathway (evasion of apoptosis) an

267 nce links KDR activation to endothelial cell mitogenesis, there is still significant uncertainty conc

268 ile cell-cell E-cadherin ligandation reduced mitogenesis, this chemoprotection was proliferation-inde

269 ry human fibroblast adhesion, migration, and mitogenesis through integrins alpha(6)beta(1), alpha(v)b

270 factor (EGF) affects cell proliferation and mitogenesis through its tyrosine kinase receptor.

271 own-regulating) abolishes TGF-beta-dependent mitogenesis, transcriptional activity, type I receptor p

272 factor-I receptor (IGF-IR) is implicated in mitogenesis, transformation, and anti-apoptosis.

273 in, Shc, is involved in cytokine production, mitogenesis, transformation, and apoptosis in different

274 n, has been found to be involved in cellular mitogenesis, tumor growth, and metastasis, in addition t

275 broad actions, including in differentiation, mitogenesis, tumor suppression, and neuronal plasticity.

276 tion of Rap1b is required for cAMP-dependent mitogenesis, tumorigenesis, and inhibition of AKT activi

277 at least in some cells, also sufficient for mitogenesis under these conditions.

278 d matricellular protein which contributes to mitogenesis via activation of Integrin-Linked Kinase (IL

279 Despite stimulation of mitogenesis via multiple signaling pathways, including s

280 rs, activation of only D(2) receptors causes mitogenesis via phosphorylation of p44/42 MAPK.

281 The most pronounced increase in mitogenesis was consistently observed for the gamma vari

282 Importantly, TGF-beta1-induced mitogenesis was markedly attenuated by inhibition of Wnt

283 d D(4) receptor agonists, respectively), and mitogenesis was measured as a function of [(3)H]thymidin

284 5-HT-induced PASMC mitogenesis was reduced by dominant-negative G(q) protei

285 ivates signaling responses and may stimulate mitogenesis, we assessed the effect of HKa binding on en

286 strictly required for the effects of cAMP on mitogenesis, we hypothesized that the Rap1 activator Epa

287 By comparison, effects of exogenous Pim-1 on mitogenesis were nominal.

288 HGF-induced MAPK phosphorylation and mitogenesis were not inhibited by vascular endothelial g

289 sed treatment with 10 pm 17beta-E2 increased mitogenesis, whereas continuous exposure to the same con

290 y role this cyclin plays in normal B-1a cell mitogenesis, whereas experiments with cyclin D3-deficien

291 cromol/L) abolished phenylephrine-stimulated mitogenesis, whereas inhibitors of other intracellular R

292 APK kinase activation but not EGF-stimulated mitogenesis, whereas SB203580 inhibited EGF-stimulated m

293 , but not SB203580, inhibited EGF-stimulated mitogenesis, whereas SP600125 did not alter the mitogeni

294 tor stimulation is known to cause fibroblast mitogenesis, which could contribute to this lesion.

295 Because of its role in mitogenesis, which is especially relevant to wound heali

296 ived growth factor-induced DNA synthesis and mitogenesis with IC(50) values of 20.4 and 27.5 nmol/L,

297 egrin receptor signals are costimulatory for mitogenesis with the T-cell receptor during T-cell activ

298 her investigated the putative role of PSM in mitogenesis with three independent experimental strategi

299 rential effect of pp120 on IGF-1 and insulin mitogenesis, with pp120 downregulating the growth-promot

300 of early gene expression and stimulation of mitogenesis without direct tyrosine phosphorylation.