IGDB.NSCLC Gene View
 
Gene Information        (help)
Gene RAPGEF1 Ensembl ENSG00000107263 Chromosome 9 Start 133441978 End 133605282
Description Rap guanine nucleotide exchange factor 1 (Guanine nucleotide-releasing factor 2)(C3G protein)(CRK SH3-binding GNRP) [Source:UniProtKB/Swiss-Prot;Acc:Q13905]
GENE RESOURCES :NUCLEOTIDE SEQUENCES :PROTEIN RESOURCES :CLINICAL RESOURCES :REFERENCES :
     HGNC : 4568
     Entrez Gene : 2889
     UCSC : uc004cbb.2
     GeneCards : 4568
     RefSeq : NM_005312
     CCDS : CCDS48047.1
     Uniprot : Q13905
     Interpro : Q13905
     OMIM : 600303
     GeneTests : RAPGEF1
     CGAP : RAPGEF1
     PMID : 7959692

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Somatic Mutaions        (help)
Lung cancer Adenocarcinoma Squamous Cell Carcinoma
Unique Mutated Samples % Mutated Total Unique
Samples
Unique Mutated
Samples
% Mutated Total Unique
Samples
Unique Mutated
Samples
% Mutated Total Unique
Samples
1 0.50 200 1 0.53 189 0 0.00 0
Sample datas
Sample Name Histology Subtype DNA Mutation Protein Mutation Mutation Description Zygosity Genomic Co-ordinates NCBI36 Pubmed
17730 AD c.117C>A p.F39L Substitution - Missense Heterozygous 9:133516105-13351610518948947

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Microarray Gene Expression Fold Change Result        (help)
( red: up-regulation / green : down-regulation when p value < 0.01)
( gray background : these probesets might have mapping problems. ref 1, ref 2)
Chip Type Probeset Adenocarcinoma Squamous Cell Carcinoma
Fold Change p value q value Fold Change p value q value
 HG_U95  36240_at  -0.46  8.06e-3  1.94e-2  -0.36  1.42e-1  2.20e-1
 HG_U133A  204543_at  -0.06  6.56e-1  7.00e-1  3.49  1.63e-75  5.95e-75
 HG_U133_Plus2  204543_at  -0.18  3.37e-1  4.27e-1  0.01  9.49e-1  9.59e-1
 HG_U133_Plus2  225738_at  -0.57  1.76e-8  1.04e-7  0.02  8.77e-1  8.99e-1
 HG_U133_Plus2  226389_s_at  -0.86  1.86e-9  1.25e-8  -0.60  3.96e-4  8.11e-4
 HG_U133_Plus2  244408_at  -0.78  8.36e-13  8.69e-12  -0.63  1.79e-8  6.52e-8
 Agilent_HS_21.6K  722  -0.03  4.61e-1  6.42e-1  -0.03  3.24e-1  4.83e-1

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Adjuvant Cisplatin/vinorelbine Treatment vs Observation Result        (help) (Pubmed)
( red: up-regulation / green : down-regulation when p value < 0.01)
( gray background color : the mapping problems of probeset. ref_1, ref_2)
Chip Type Probeset Adenocarcinoma Squamous Cell Carcinoma
Fold Change p value q value Fold Change p value q value
 HG_U133A  204543_at  -0.29  5.09e-1  9.31e-1  -0.12  6.35e-1  1.00e+0

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Microarray Sample Data        (help)
( The log2 value of tumor samples )
(Average : Average log2 value from Normal Samples.)
        HG_U95 - 36240_at    (back)       Save as a PNG file. Save as a PDF file. Save as a PS file.
Gene expression figure

        HG_U133A - 204543_at    (back)       Save as a PNG file. Save as a PDF file. Save as a PS file.
Gene expression figure

        HG_U133_Plus2 - 204543_at    (back)       Save as a PNG file. Save as a PDF file. Save as a PS file.
Gene expression figure

        HG_U133_Plus2 - 225738_at    (back)       Save as a PNG file. Save as a PDF file. Save as a PS file.
Gene expression figure

        HG_U133_Plus2 - 226389_s_at    (back)       Save as a PNG file. Save as a PDF file. Save as a PS file.
Gene expression figure

        HG_U133_Plus2 - 244408_at    (back)       Save as a PNG file. Save as a PDF file. Save as a PS file.
Gene expression figure

        Agilent_HS_21.6K - 722    (back)       Save as a PNG file. Save as a PDF file. Save as a PS file.
Gene expression figure

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Cancer Gene Index        (help)

If 0 entry was found, please remove the search key "lung cancer".
Keyword DiseaseData Statement PubMed Organism
c3g non-small cell lung cancers Amplification, up-regulation and over-expression of C3G (CRK SH3 domain-binding guanine nucleotide-releasing factor) in non-small cell lung cancers. 15138850 Human
c3g tumors We document here the amplification of C3G in five of 18 primary non-small cell lung cancers examined and its increased expression in 18 of 28 tumors in comparison to corresponding non-cancerous lung tissues. 15138850 Human
c3g non-small cell lung cancers We document here the amplification of C3G in five of 18 primary non-small cell lung cancers examined and its increased expression in 18 of 28 tumors in comparison to corresponding non-cancerous lung tissues. 15138850 Human
c3g cancer Immunohistochemical staining revealed prominent C3G protein in the cytoplasm of cancer cells, associated with faint staining at the nucleolar membrane, but C3G was not detectable in normal bronchial mucoepithelial cells or in broncholoalveolar cells of th 15138850 Human
c3g casitas b-lineage lymphoma This leads to antigen receptor-independent phosphorylation of Cbl (Casitas B lineage lymphoma) and C3G. 11489945 Human
c3g tumor Similarly to previously identified Rap GEFs, C3G and Smg GDS, each of the newly identified exchange factors promoted the activation of Elk-1 in the LNCaP prostate tumor cell line where B-Raf can couple Rap1 to the extracellular receptor-activated kinase c 10934204 Human
c3g prostate tumor Similarly to previously identified Rap GEFs, C3G and Smg GDS, each of the newly identified exchange factors promoted the activation of Elk-1 in the LNCaP prostate tumor cell line where B-Raf can couple Rap1 to the extracellular receptor-activated kinase c 10934204 Human
c3g myelogenous leukemia In addition, lysates from leukemic cells of P190 BCR/ABL transgenic mice and of the myelogenous leukemia cell line K562 contained tyrosine-phosphorylated C3G and activated Rap1. 15982636 Human
c3g chronic myeloid leukemia Characterization of p87C3G, a novel, truncated C3G isoform that is overexpressed in chronic myeloid leukemia and interacts with Bcr-Abl. 16443220 Human
c3g chronic myeloid leukemia (cml) A novel C3G isoform, designated p87C3G, lacking the most amino terminal region of the cognate protein has been found to be overexpressed in two CML cell lines, K562 and Boff 210, both expressing Bcr-Abl p210. p87C3G expression is also highly augmented in 16443220 Human
c3g cml A novel C3G isoform, designated p87C3G, lacking the most amino terminal region of the cognate protein has been found to be overexpressed in two CML cell lines, K562 and Boff 210, both expressing Bcr-Abl p210. p87C3G expression is also highly augmented in 16443220 Human
c3g chronic myeloid leukemia These results indicate that p87C3G overexpression is linked to CML phenotype and that p87C3G may exert productive functional interactions with Bcr-Abl signaling components suggesting the implication of this C3G isoform in the pathogenesis of chronic myelo 16443220 Human
c3g cml These results indicate that p87C3G overexpression is linked to CML phenotype and that p87C3G may exert productive functional interactions with Bcr-Abl signaling components suggesting the implication of this C3G isoform in the pathogenesis of chronic myelo 16443220 Human
c3g cervical squamous cell carcinoma Inactivation of Crk SH3 domain-binding guanine nucleotide-releasing factor (C3G) in cervical squamous cell carcinoma. 16681758 Human
c3g cervical squamous cell carcinomas Here we examined the C3G expression in cervical squamous cell carcinomas and found a marked decrease in the expression of C3G in a high incidence of said samples. 16681758 Human
c3g cervical squamous cell carcinoma These results indicate that inactivation of C3G by de novo methylation plays an important role in the development of cervical squamous cell carcinoma. 16681758 Human
c3g oncogene BACKGROUND: Proline-rich segments in the guanine nucleotide exchange factor C3G bind much more strongly to the N-terminal Src homology 3 domain (SH3-N) of the proto-oncogene product c-Crk than to other SH3 domains. 7735837 Human
c3g oncogenes Overexpression in NIH3T3 cells of a full-length C3G cDNA isolated from human placenta markedly reduced the focus forming activity of cotransfected, malignantly activated, ras oncogenes (5-7-fold). 9482107 Human
c3g oncogene Surprisingly, as opposed to Rap1A, which has no effect on Raf-1 oncogene-mediated transformation, C3G also reduced dramatically (6-8-fold) the number of v-raf-induced foci in transfected NIH3T3 cells. 9482107 Human
c3g oncogenes In contrast, a C3G mutant (C3G Cat), containing the catalytic domain only but lacking the rest of the N-terminal sequences, did not have any inhibitory effect on transformation mediated by the oncogenes tested. 9482107 Human
c3g oncogene The utility of this technique is illustrated through the preparation of an array of proline-rich sequences based on the exchange factor C3G, one of the natural ligands of the N-terminal SH3 domain from the proto-oncogene, c-Crk. 9585562 Human
c3g oncogene Crk activation of JNK via C3G and R-Ras. v-crk is an oncogene identified originally in CT10 chicken tumor virus. 10777559 others
c3g oncogenic C3G, a guanine nucleotide exchange factor (GEF) for Rap1 and R-Ras, is postulated to transduce the oncogenic signal of v-Crk to c-Jun kinase (JNK). 10777559 others
c3g oncogene C3G-mediated suppression of oncogene-induced focus formation in fibroblasts involves inhibition of ERK activation, cyclin A expression and alterations of anchorage-independent growth. 15077165 Mouse
c3g oncogenes We showed previously that exogenous overexpression of C3G, a guanine nucleotide releasing factor (GEF) for Rap1 and R-Ras proteins, blocks the focus-forming activity of cotransfected, activated, sis, ras and v-raf oncogenes in NIH 3T3 cells. 15077165 Mouse
c3g oncogenic Using full-length C3G and C3GDeltaCat mutant, lacking catalytic domain, we showed here that overexpression of cotransfected C3G or C3GDeltaCat inhibited oncogenic Hraslys12-mediated phosphorylation of ERK, without altering Ras and Raf-1 kinase activation. 15077165 Mouse
c3g oncogenic We also showed that, overexpressed C3G and C3GdeltaCat inhibited the viability of oncogenic Ras-induced colonies in soft agar, indicating that C3G interferes with the anchorage-independent growth of Ras-transformed cells in a Rap1-independent manner. 15077165 Mouse
c3g oncogenic Altogether, our results indicate that C3G interferes with at least two separate aspects of oncogenic transformation - cell cycle progression and loss of contact inhibition - and that these inhibitory effects probably account for its transformation suppres 15077165 Mouse
c3g small cell lung cancers We document here the amplification of C3G in five of 18 primary non-small cell lung cancers examined and its increased expression in 18 of 28 tumors in comparison to corresponding non-cancerous lung tissues. 15138850 Human
c3g carcinogenesis These data indicate that amplification and increased expression of the C3G gene may play some role in human lung carcinogenesis through derangement of the CRK-Rap1 signaling pathway. 15138850 Human
c3g leukemia These data suggest a role for C3G-mediated Rap1 activation in Bcr/Abl-induced leukemia development. 15982636 Human

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