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1 ocation in acute promyelocytic leukemia is a growth suppressor.
2 onal regulation of the RPP5 gene, encoding a growth suppressor.
3  thereby keeping pRb in its active form as a growth suppressor.
4 , supporting the role of LSP1 as a selective growth suppressor.
5 inson's disease, and was first reported as a growth suppressor.
6 9, as an IFN/all-trans retinoic acid-induced growth suppressor.
7    GRIM-19 is an IFN/retinoic acid-regulated growth suppressor.
8 istent with a role for endogenous Grb10 as a growth suppressor.
9  of Protein 4.1B to function as a meningioma growth suppressor.
10 uces the expression of GADD45A, a known cell growth suppressor.
11  suggesting that it also has properties of a growth suppressor.
12 to oppose inflammatory pathways and act as a growth suppressor.
13 hat is dominant over its potential role as a growth suppressor.
14 in-oral-cancer-1 (DOC-1), a highly conserved growth suppressor.
15 d is a strong candidate, since it is a known growth suppressor.
16 onsive genes, induce apoptosis, and act as a growth suppressor.
17  p16beta can act as a functional glioma cell growth suppressor.
18 s that limit Wnt signals and may function as growth suppressors.
19 ferons (IFNs) and retinoids are potent tumor growth suppressors.
20 from the maternally derived genome should be growth suppressors.
21 nd the RECQ4 helicases--the Arabidopsis slow growth suppressor 1 (Sgs1)/Bloom syndrome protein (BLM)
22 the chick homologue of mammalian leprecan or growth suppressor 1.
23  processes such as proliferation, evasion of growth suppressors, activating metastasis, and metabolic
24 ith antibody to DLC-1 and the possible tumor growth suppressor activity of DLC-1 was investigated by
25                                    Thus, the growth suppressor activity of E-cadherin is adhesion ind
26                                  The loss of growth suppressor activity when the Cdk2-repressor domai
27  general repressor activity, and most of the growth suppressor activity.
28 1 alpha binds necdin, a nuclear protein with growth suppressor activity.
29 ding to HRS does not negatively regulate HRS growth suppressor activity.
30 -cycle regulator, originally identified as a growth suppressor and a prognostic marker for human oral
31 elocytic leukemia protein PML is a tumor and growth suppressor and plays an important role in a multi
32       Together, the results suggest that the growth suppressor and transcriptional activator function
33  observations suggest that LATS1 is a potent growth suppressor and, like other tumor suppressors, it
34  PML-homo and hetero interactions conferring growth suppressor, apoptotic and anti-viral activities.
35 sting that GAP43 functions as a novel glioma growth suppressor by modulating mitogenic signaling path
36  a transcription factor, functions as a cell growth suppressor by negatively regulating the expressio
37 hematopoietic progenitors and functions as a growth suppressor by repressing cyclin A2 and other targ
38 tent with the hypothesis that GPC3 acts as a growth suppressor by sequestering or downregulating an I
39                                              Growth suppressor c-Abl interacts with p53 in response t
40 ugh different mechanisms, and a constitutive growth suppressor can be generated through the combined
41             These data have demonstrated the growth-suppressor characteristics of PTPRO that are uniq
42 for deletion or substitution mutation in the growth suppressor domains of MDM2 in several breast canc
43            In addition, RGS2 functioned as a growth suppressor for androgen-independent LNCaP cells w
44 ecific missense mutations within the minimal growth suppressor fragment of Protein 4.1B (DAL-1, diffe
45 onstrate a new approach for the isolation of growth suppressors from cDNA libraries, and identify a p
46 lin A/E-CDK2 sites, negatively regulates the growth suppressor function associated with the N-termina
47 s a new target of miR-335 that regulates its growth suppressor function by complex crosstalk with oth
48                    Our data suggest that the growth suppressor function of BRCA1 depends, at least in
49 ent kinase inhibitors, and activation of the growth suppressor function of pocket proteins.
50 main activates, rather than inactivates, the growth suppressor function of pRb.
51 t binding to 14-3-3 is not essential for the growth suppressor function of Protein 4.1B in meningioma
52 of the full-length DAL-1 molecule eliminated growth suppressor function, as measured by thymidine inc
53 lity to form colonies in vitro, suggesting a growth suppressor function.
54 tional activity, which may contribute to its growth suppressor function.
55 sed a similar functional assay to localize a growth suppressor gene for the RD cell line centromeric
56 a prove that wild-type IGFIIR functions as a growth suppressor gene in colorectal cancer cells and pr
57 hese data suggest that SLC5A8 functions as a growth suppressor gene in vitro and that it is silenced
58         These data therefore implicate a new growth suppressor gene involved in breast cancer that is
59  H19, an untranslated RNA that is a putative growth suppressor gene regulating IGF-II; (c) p57KIP2, a
60               We have further localized this growth suppressor gene to 17q24-q25 by transfer of chrom
61              Though BRCA1 is thought to be a growth suppressor gene, no change in BRCA1 protein level
62 rt for the hypothesis that IGFIIR is a human growth suppressor gene.
63 ossible mechanisms including reexpression of growth suppressor genes and formation of covalent adduct
64 modify the expression of proto-oncogenes and growth suppressor genes during embryogenesis.
65 ones selected for by loss of dominant-acting growth suppressor genes.
66                              p12(DOC-1) is a growth suppressor identified and isolated from normal ke
67 d Mortality-19) was originally isolated as a growth suppressor in a genome-wide knockdown screen with
68 t in vivo evidence that LRIG1 functions as a growth suppressor in breast cancer.
69 vide functional validation for its role as a growth suppressor in EGFR-mutant lung adenocarcinoma.
70 vations suggest that C-CAM1 may be a general growth suppressor in epithelial cells.
71 vide a functional test of its candidacy as a growth suppressor in glioma cells.
72 activation of this gene and that it can be a growth suppressor in human gliomas.
73 r the first time that nSMase2 functions as a growth suppressor in MCF7 cells, linking confluence to t
74 mation, suggesting that it may function as a growth suppressor in normal brain cells.
75 her, these data indicate that PML is a tumor growth suppressor in prostate cancer and that Ad-PML may
76 he first time that N-cadherin functions as a growth suppressor in the context of oncogenic K-ras.
77 ngs demonstrate that Mzf1 can act as a tumor/growth suppressor in the hemopoietic compartment.
78 are members of the HIPPO pathway that act as growth suppressors in adult proliferative diseases.
79 t these miRs function as metastasis (but not growth) suppressors in prostate cancer.
80                     p12(CDK2-AP1) (p12) is a growth suppressor isolated from normal keratinocytes.
81                              p12(DOC-1) is a growth suppressor isolated from normal keratinocytes.
82 eveal the post-translational regulation of a growth suppressor like CHK2 within the microenvironment
83                                  NKX3.1 is a growth suppressor, mediator of apoptosis, inducer of ant
84                                          The growth suppressor MST1 kinase modulates androgen-depende
85  and were severely impaired for growth; recB growth suppressor mutants arose at high frequencies.
86                       Here we characterize a growth suppressor mutation in eIF2beta that prevents eIF
87 All-trans retinoic acid (RA) is an effective growth suppressor of CA-OV3 cells but not SK-OV3 cells.
88 inoic acid (RA) combination is a more potent growth suppressor of human tumor xenografts in vivo than
89 RCA1a and BRCA1b splice variants function as growth suppressors of human breast cancer cells.
90 ed 17b-estradiol from a growth-promoter to a growth-suppressor, offering a targetable therapeutic vul
91 within 8 weeks, suggesting the presence of a growth suppressor on chromosome 17.
92 ation might be specifically repressed by the growth suppressor p107 through direct interaction with B
93 ogenes and indirectly by down-regulating the growth suppressor p21(WAF1/CIP1).
94         We have investigated the role of the growth suppressor p27(Kip1) (p27) on endothelial cell fu
95 restoring normal activation of the Hippo-YAP growth-suppressor pathway.
96        Although deregulation of the putative growth suppressor PML and delocalization of other nuclea
97                                          The growth suppressor promyelocytic leukemia protein (PML) i
98 onsistent with a role for the retinoblastoma growth suppressor protein in protein kinase C-induced ap
99 ent kinase inhibitors and the retinoblastoma growth suppressor protein.
100  phosphorylation status of the pRB family of growth suppressor proteins is regulated in a cell cycle
101 med acquisition of the endogenously produced growth suppressor PTEN.
102      We show that both PML and Tif1alpha are growth suppressors required for the growth-inhibitory ac
103 nt to sustain proliferative signaling, evade growth suppressors, resist cell death, promote replicati
104 s sustained proliferation, refractoriness to growth suppressors, resistance to cell death or aberrant
105 afficking events; and (f) down-regulation of growth suppressors, such as the Prader-Willi gene NECDIN
106 ation of PRDX2 as an epigenetically silenced growth suppressor, suggesting a possible role of ROS in
107  protein (RB110), is a more potent tumor and growth suppressor than RB110.
108 e, we found that knock-down of KLF9, an axon growth suppressor that is normally upregulated 250-fold
109 but frequently gave rise to spontaneous slow growth suppressors that segregated as single-gene mutati
110 entified, including inactivation of cellular growth suppressors through direct interaction with SV40
111               To conclude, JunD changed from growth suppressor to growth promoter when its binding to
112 ting that the polyploid state functions as a growth suppressor to restrict proliferation by the major
113 er we reported the isolation of GRIM-19 as a growth suppressor using a genome-wide expression knockdo
114 We have previously isolated GRIM-19, a novel growth suppressor, using a genetic method.
115 te the basis for these defects, a screen for growth suppressors was performed.
116 on as a potent transcriptional repressor and growth suppressor, while the Mxi1-WR protein lacks these

 
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