H-ras gene

関: H-ras oncogene、Ha-ras gene、Ha-ras oncogene、K-ras gene、K-ras oncogene、Ki-ras gene、Ki-ras oncogene、N-ras gene、N-ras oncogene、ras gene、ras oncogene

WordNet

(genetics) a segment of DNA that is involved in producing a polypeptide chain; it can include regions preceding and following the coding DNA as well as introns between the exons; it is considered a unit of heredity; "genes were formerly called factors" (同)cistron, factor
the 8th letter of the Roman alphabet (同)h
informal term for information; "give me the gen on your new line of computers"

PrepTutorEJDIC

遺伝子
hydrogenの化学記号
鉛筆の硬度 / 《俗》heroin
roentgen / recto

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 甲状腺結節および非髄様甲状腺癌におけるオンコジーンおよび腫瘍抑制遺伝子 oncogenes and tumor suppressor genes in thyroid nodules and nonmedullary thyroid cancer
2. 脂腺母斑および脂腺母斑症候群 nevus sebaceous and nevus sebaceous syndrome
3. スピッツ母斑様色素細胞性腫瘍：スピッツ母斑および異型スピッツ腫瘍：臨床的特徴、
診断および管理 spitzoid melanocytic neoplasms spitz nevus and atypical spitz tumors
4. ケラトアカントーマ：疫学、危険因子、および診断 keratoacanthoma epidemiology risk factors and diagnosis
5. 進行非小細胞肺癌に対する遺伝子型による個別治療 personalized genotype directed therapy for advanced non small cell lung cancer

English Journal

Adrenomedullin is a therapeutic target in colorectal cancer.

Wang L1, Gala M, Yamamoto M, Pino MS, Kikuchi H, Shue DS, Shirasawa S, Austin TR, Lynch MP, Rueda BR, Zukerberg LR, Chung DC.Author information 1Gastrointestinal Unit Massachusetts General Hospital, Harvard Medical School, Boston, MA; Department of Gastroenterology Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.AbstractThe KRAS oncogene influences angiogenesis, metastasis and chemoresistance in colorectal cancers (CRCs), and these processes are all enhanced in hypoxic conditions. To define functional activities of mutant KRAS in a hypoxic microenvironment, we first performed cDNA microarray experiments in isogenic DKs5 and DKO3 colon cancer cell lines that differ only by their expression of mutant KRAS (K-ras(D13)). Adrenomedullin (ADM) was identified as one of the most significantly upregulated genes in DKs5 cells that express the KRAS oncogene in hypoxia (3.2-fold, p = 1.47 × 10(-5)). Ectopic expression of mutant KRAS (K-ras(V12)) in Caco-2 cells (K-ras(WT)) induced ADM, whereas selective knockdown of mutant KRAS alleles (K-ras(D13) or K-ras(V12)) in HCT116, DLD1 and SW480 colon cancer cells suppressed the expression of ADM in hypoxia. Knockdown of ADM in colon tumor xenografts blocked angiogenesis and stimulated apoptosis, resulting in tumor suppression. Furthermore, ADM also regulated colon cancer cell invasion in vitro. Among 56 patients with CRC, significantly higher expression levels of ADM were observed in samples harboring a KRAS mutation. Collectively, ADM is a new target of oncogenic KRAS in the setting of hypoxia. This observation suggests that therapeutic targets may differ depending upon the specific tumor microenvironment.
International journal of cancer. Journal international du cancer.Int J Cancer.2014 May 1;134(9):2041-50. doi: 10.1002/ijc.28542. Epub 2013 Nov 7.
The KRAS oncogene influences angiogenesis, metastasis and chemoresistance in colorectal cancers (CRCs), and these processes are all enhanced in hypoxic conditions. To define functional activities of mutant KRAS in a hypoxic microenvironment, we first performed cDNA microarray experiments in isogenic
PMID 24519534

RASSF1A promotes apoptosis and suppresses the proliferation of ovarian cancer cells.

Fu L, Zhang S.Author information Department of Gynaecology and Obstetrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.AbstractAs the most lethal gynecological malignancy, ovarian cancer has attracted much attention over the past few decades; however, the early detection of this malignancy has been largely unsuccessful. The aim of this study was to determine the effects of Ras-association domain family 1, isoform A (RASSF1A) on ovarian cancer and to elucidate the molecular mechanisms responsible for these effects. The expression of RASSF1A in different ovarian cancer cells was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The morphology, structure, apoptosis and proliferation of differently treated SKOV-3 cells were then analyzed using a fluorescence microscope, transmission electron microscope, flow cytometer and by western blot analysis, respectively. Moreover, the GSE14407 affymetrix microarray data were downloaded from the Gene Expression Omnibus database and the expression of RASSF1A was quantified by Spotfire DecisionSite software. A RASSF1A related protein-protein interaction (PPI) network was then constructed using STRING and Cytoscape software. Finally, DAVID was utilized to perform KEGG pathway enrichment analysis of the network. RASSF1A was expressed in the HO8910, HO8910PM cells and the SKOV-3 cells transfected with RASSF1A, whereas it was absent in the other SKOV-3 cells and OVCAR-3 cells. Additionally, compared with the other SKOV-3 cells, the nucleus of SKOV-3 cells transfected with RASSF1A was vacuolated, apoptosis was increased, and the expression of cyclin D1 and survivin was decreased (P<0.05), and that of p27 and caspase-3 was increased (P<0.01). Additionally, 10 genes, including serine/threonine kinase (STK)3, STK4, Harvey rat sarcoma viral oncogene homolog (HRAS) and cell division cycle 20 (CDC20), were found to have close interactions with RASSF1A in the PPI network. Finally, a total of 8 enriched pathways, such as bladder cancer, non-small cell lung cancer and pathways in cancer were identified. To our knowledge, this is the first study to explore the biological functions and the underlying mechanisms of action of RASSF1A in the development of ovarian cancer. Our findings may provide a novel therapeutic target for ovarian cancer.
International journal of molecular medicine.Int J Mol Med.2014 May;33(5):1153-60. doi: 10.3892/ijmm.2014.1671. Epub 2014 Feb 25.
As the most lethal gynecological malignancy, ovarian cancer has attracted much attention over the past few decades; however, the early detection of this malignancy has been largely unsuccessful. The aim of this study was to determine the effects of Ras-association domain family 1, isoform A (RASSF
PMID 24573512

Behavioral Profile in RASopathies.

Alfieri P1, Piccini G, Caciolo C, Perrino F, Gambardella ML, Mallardi M, Cesarini L, Leoni C, Leone D, Fossati C, Selicorni A, Digilio MC, Tartaglia M, Mercuri E, Zampino G, Vicari S.Author information 1Dipartimento di Neuroscienze, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.AbstractHere, we describe neurobehavioral features in patients with RASopathies (i.e., Noonan syndrome, LEOPARD syndrome, Costello syndrome, and cardiofaciocutaneous syndrome), developmental disorders caused by mutations in genes coding transducers participating in the RAS-MAPK signaling cascade. Parents of 70 individuals with a RASopathy were asked to fill out the following questionnaires: Child Behavior Checklist (CBCL), Social Communication Questionnaire version lifetime (SCQ-L), and Modified Checklist for Autism in toddlers (M-CHAT). Data analysis indicated high rates of internalizing (37%) and externalizing problems (31%) on CBCL. Scores over the cut-off were documented in 64% of patients with cardiofaciocutaneous syndrome, 44% with Costello syndrome, and 12% with Noonan syndrome on SCQ-L/M-CHAT. Our findings indicate that mutations promoting dysregulation of the RAS-MAPK cascade mark an increased psychopathological risk and highlight that autistic-like behavior could be underdiagnosed in patients with RASopathies. © 2014 Wiley Periodicals, Inc.
American journal of medical genetics. Part A.Am J Med Genet A.2014 Apr;164(4):934-42. doi: 10.1002/ajmg.a.36374. Epub 2014 Jan 23.
Here, we describe neurobehavioral features in patients with RASopathies (i.e., Noonan syndrome, LEOPARD syndrome, Costello syndrome, and cardiofaciocutaneous syndrome), developmental disorders caused by mutations in genes coding transducers participating in the RAS-MAPK signaling cascade. Parents of
PMID 24458522

Japanese Journal

Increased H-ras mutation frequency in mammary tumors of rats initiated with N-methyl-N-nitrosourea (MNU) and treated with acrylamide

Journal of toxicological sciences 34(4), 407-412, 2009-08-01
NAID 110007359659

ヒトパピローマウイルスによる発がんの分子機構

ウイルス 58(2), 141-154, 2008
NAID 130004470914

Analyses of Novel Prognostic Factors in Neuroblastoma Patients(Molecular and Cell Biology)

Biological & pharmaceutical bulletin 30(12), 2294-2299, 2007-12-01
NAID 110006546428

Related Links

HRAS Gene - GeneCards | RASH Protein | RASH Antibody

Selected SIMAP similar genes for HRAS Gene using alignment to 2 proteins: RASH_HUMAN P78460_HUMAN N-ras K-RAS c-bas/has KRAS K-ras H-RAS NRAS RAP1B RALA RIT2 RAP1A RIT1 RAP2A RALB RRAS2 RRAS ...

H-Ras siRNA (h), shRNA and Lentiviral Particle Gene Silencers

10 µM, 50-100 transfections siRNA products generally consist of pools of three to five target-specific 19-25 nt siRNAs designed to knockdown gene expression for independent verification of H-Ras gene silencing results, individual ...

Related Pictures

★リンクテーブル★

リンク元	「ras遺伝子」「H-ras遺伝子」「N-ras gene」
関連記事	「RAS」「H」

「ras遺伝子」

英: ras gene
関: H-ras gene、H-ras oncogene、Ha-ras gene、Ha-ras oncogene、K-ras gene、K-ras oncogene、Ki-ras gene、Ki-ras oncogene、N-ras gene、N-ras oncogene、ras oncogene

低分子量Gタンパク質をコードする癌原遺伝子の一種

「H-ras遺伝子」

英: H-ras gene
関: K-ras遺伝子、N-ras遺伝子、ras遺伝子、K-ras癌遺伝子、H-ras癌遺伝子、Ha-ras遺伝子、Ha-ras癌遺伝子、Ki-ras遺伝子、Ki-ras癌遺伝子、ras癌遺伝子、N-ras癌遺伝子

「N-ras gene」

関: H-ras gene、H-ras oncogene、Ha-ras gene、Ha-ras oncogene、K-ras gene、K-ras oncogene、Ki-ras gene、Ki-ras oncogene、N-ras oncogene、ras gene、ras oncogene

「RAS」

「H」

　　　

「https://meddic.jp/index.php?title=H-ras_gene&oldid=228368」から取得

.