The Brm gene suppressed at the post-transcriptional level in various human cell lines is inducible by transient HDAC inhibitor treatment, which exhibits antioncogenic potential.
about
HDAC Inhibitors as Epigenetic Regulators of the Immune System: Impacts on Cancer Therapy and Inflammatory DiseasesThe disparate origins of ovarian cancers: pathogenesis and prevention strategies.The role of the SWI/SNF chromatin remodeling complex in maintaining the stemness of glioma initiating cellsThe silencing of the SWI/SNF subunit and anticancer gene BRM in Rhabdoid tumorsModulation of Brahma expression by the mitogen-activated protein kinase/extracellular signal regulated kinase pathway is associated with changes in melanoma proliferation.SNF5/INI1 deficiency redefines chromatin remodeling complex composition during tumor development.Insertion/deletion polymorphisms in the promoter region of BRM contribute to risk of hepatocellular carcinoma in Chinese populations.Identification of differentially expressed genes in HPV-positive and HPV-negative oropharyngeal squamous cell carcinomas.Cathepsin E is a marker of gastric differentiation and signet-ring cell carcinoma of stomach: a novel suggestion on gastric tumorigenesis.Ablation of Kcnj10 expression in retinal explants revealed pivotal roles for Kcnj10 in the proliferation and development of Müller glia.Complex alternative splicing of the smarca2 gene suggests the importance of smarca2-B variantsGli regulates MUC5AC transcription in human gastrointestinal cellsOxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy.Epigenetically maintained SW13+ and SW13- subtypes have different oncogenic potential and convert with HDAC1 inhibition.Two novel BRM insertion promoter sequence variants are associated with loss of BRM expression and lung cancer risk.Concomitant loss of SMARCA2 and SMARCA4 expression in small cell carcinoma of the ovary, hypercalcemic typeEpigenetic aberrations and cancer.Discovery of BRM Targeted Therapies: Novel Reactivation of an Anti-cancer GeneDual loss of the SWI/SNF complex ATPases SMARCA4/BRG1 and SMARCA2/BRM is highly sensitive and specific for small cell carcinoma of the ovary, hypercalcaemic type.Loss of switch/sucrose non-fermenting complex protein expression is associated with dedifferentiation in endometrial carcinomas.Hijacking the chromatin remodeling machinery: impact of SWI/SNF perturbations in cancer.Two BRM promoter insertion polymorphisms increase the risk of early-stage upper aerodigestive tract cancers.Chromatin regulators with tumor suppressor properties and their alterations in human cancers.Nucleolin is required for efficient nuclear egress of herpes simplex virus type 1 nucleocapsids.Beyond Mutations: Additional Mechanisms and Implications of SWI/SNF Complex Inactivation.Analysis of Müller glia specific genes and their histone modification using Hes1-promoter driven EGFP expressing mouseEpigenomic regulation of oncogenesis by chromatin remodeling.The miR-199a/Brm/EGR1 axis is a determinant of anchorage-independent growth in epithelial tumor cell lines.Phosphorylation of herpes simplex virus 1 dUTPase upregulated viral dUTPase activity to compensate for low cellular dUTPase activity for efficient viral replication.Identifying targets for the restoration and reactivation of BRM.Association of two BRM promoter polymorphisms with head and neck squamous cell carcinoma risk.HDAC inhibitors regulate claudin-1 expression in colon cancer cells through modulation of mRNA stability.Valproic acid causes dose- and time-dependent changes in nuclear structure in prostate cancer cells in vitro and in vivo.Vectors expressing efficient RNA decoys achieve the long-term suppression of specific microRNA activity in mammalian cells.MiR-199a Inhibits Secondary Envelopment of Herpes Simplex Virus-1 Through the Downregulation of Cdc42-specific GTPase Activating Protein Localized in Golgi Apparatus.Frequent co-inactivation of the SWI/SNF subunits SMARCB1, SMARCA2 and PBRM1 in malignant rhabdoid tumours.Pharmacologic reversal of epigenetic silencing of the anticancer protein BRM: a novel targeted treatment strategy.BRM Promoter Polymorphisms and Survival of Advanced Non-Small Cell Lung Cancer Patients in the Princess Margaret Cohort and CCTG BR.24 Trial.BMP signaling participates in late phase differentiation of the retina, partly via upregulation of Hey2.The spatial patterning of mouse cone opsin expression is regulated by bone morphogenetic protein signaling through downstream effector COUP-TF nuclear receptors.
P2860
Q26739120-6AC14FA0-2539-484A-B142-FBF019D80CCFQ30240709-8B64F92B-DA84-4FD2-BC7C-44101EFE41C5Q33678542-F0D1D1CE-3DE6-42A2-8583-AEC58AD13383Q34423814-7DD7F040-C538-43F1-81A0-F2560C2F0B65Q34459131-C6FD30FF-5FDA-4709-9622-2D8F8E013725Q34518342-BF539C65-6E6A-4E00-AAB3-7533E8A910D5Q34566605-770CBC9D-5360-4D1B-AA9F-669A96C3ADA2Q34578434-CA1A843D-EE72-4247-937D-C42BB586982AQ34602612-A974BCBC-E0D8-4E54-A59A-7E075388BE5CQ35070409-0586E0D5-1327-47D8-AB6A-DC71CDD70E60Q35142978-FA8C653E-DF52-4E01-9DFB-7B16DAC9B45CQ35233795-7BD3C197-2630-462C-A272-C09ADD7A4A4EQ35841917-1B3DBA46-DFED-47C4-8A91-3C67E8C76D2BQ36020172-204421CE-7D08-4731-8EFD-D2F0089EA334Q36103995-9DA624CA-A07E-4699-8A8F-1473DAEB08A1Q36420683-1710125E-2EDE-43B1-ADC9-05E1445A1AA9Q36648081-E83217CA-F600-4B4B-AFEC-5D8CEA609B4BQ36737338-E717AB76-617D-4F8F-BCDB-02A14A1B2A57Q36800071-1FE14088-885E-4831-9369-88C93911FE6FQ37166723-9D0E4EE3-7628-4975-A44B-FA4A7E6983D4Q37618471-D5CB4387-A167-42BF-B37D-6D5207A5F4D4Q37703407-D05AB598-D60D-439A-9E6A-81DAC192EA87Q38058125-3AAA530F-3164-4F50-8A96-38C31A863AF7Q38348401-AA66E139-1EA5-401E-8E3D-426FC1CAFC9BQ38379487-49004362-1520-46CB-87CA-E39FC4CCF662Q38432413-5945BE1D-DA31-4B96-AC53-6914863221C3Q38709544-7F0BD2E8-7378-45FF-AF23-1E0A19B6A97CQ38910598-A7DA23FC-1356-40DB-A51A-06DC9E9E3ABAQ39001555-3C08DE3B-BE0A-4832-861C-68EAD1D42890Q39176522-44514039-6E6E-4555-AD9F-79C62D24F451Q39209851-E958ADAA-786A-47C9-BCF4-08FF7B1781A0Q39780639-8E1D7B04-233C-43B7-A01F-E1752AFFB00FQ39860046-B4C25193-9EF7-474D-BCB3-A976411C8DD1Q39882902-2246A940-E496-4592-8AE6-0DBB0E75AC82Q40104837-9F9DC6C0-05FF-4980-A3AB-6A31581A71F2Q41703426-9F50141E-BE77-4EA6-A447-7D626B97B611Q41981592-7DA3AD5B-F09F-4F5D-9053-8558C145D16DQ42774884-9B0D84EF-D8A3-4151-AAFB-DB9F1F9D56ADQ42801760-05F2C5D1-3DBD-4036-A536-6B8597D329F9Q42957348-5F94285F-DFEA-4D14-9E9C-76C529D3BB3D
P2860
The Brm gene suppressed at the post-transcriptional level in various human cell lines is inducible by transient HDAC inhibitor treatment, which exhibits antioncogenic potential.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
2005年论文
@zh
2005年论文
@zh-cn
name
The Brm gene suppressed at the ...... ibits antioncogenic potential.
@en
type
label
The Brm gene suppressed at the ...... ibits antioncogenic potential.
@en
prefLabel
The Brm gene suppressed at the ...... ibits antioncogenic potential.
@en
P2093
P2860
P356
P1433
P1476
The Brm gene suppressed at the ...... ibits antioncogenic potential.
@en
P2093
Hirotaka Watanabe
Masao Ichinose
Masao Omata
Mitsue Yamamichi-Nishina
Nao Kobayashi
Naohisa Yahagi
Nobutake Yamamichi
Satoko Kimura
Shigeru Minoguchi
P2860
P2888
P304
P356
10.1038/SJ.ONC.1208716
P407
P577
2005-08-01T00:00:00Z
P5875
P6179
1008034904