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The product of CHD4 belongs to the SNF2/RAD54 helicase family.
Showing 10 out of 94 products:
Human Polyclonal CHD4 Primary Antibody für ICC, IF - ABIN2668534
Curtis, Griffin: The chromatin-remodeling enzymes BRG1 and CHD4 antagonistically regulate vascular Wnt signaling. in Molecular and cellular biology 2012
Show all 4 Pubmed References
Human Polyclonal CHD4 Primary Antibody für IP, PLA - ABIN252858
Ma, Lin, Bartolomei, Schultz: Metastasis tumor antigen 2 (MTA2) is involved in proper imprinted expression of H19 and Peg3 during mouse preimplantation development. in Biology of reproduction 2010
Human Polyclonal CHD4 Primary Antibody für IP, WB - ABIN252859
Gu, Hu, Ebrahem, Crabb, Mahfouz, Radivoyevitch, Crabb, Saunthararajah: Runx1 regulation of Pu.1 corepressor/coactivator exchange identifies specific molecular targets for leukemia differentiation therapy. in The Journal of biological chemistry 2014
Human Polyclonal CHD4 Primary Antibody für IP, WB - ABIN252857
Shakya, Kang, Chumley, Williams, Tantin: Oct1 is a switchable, bipotential stabilizer of repressed and inducible transcriptional states. in The Journal of biological chemistry 2011
Human Monoclonal CHD4 Primary Antibody für IHC (p), ELISA - ABIN560357
Nishibuchi, Shibata, Hayakawa, Hayakawa, Ohtani, Sinmyozu, Tagami, Nakayama: Physical and functional interactions between the histone H3K4 demethylase KDM5A and the nucleosome remodeling and deacetylase (NuRD) complex. in The Journal of biological chemistry 2014
Fruit Fly (Drosophila melanogaster) Monoclonal CHD4 Primary Antibody für IP, WB - ABIN2668526
Murawska, Kunert, van Vugt, Längst, Kremmer, Logie, Brehm: dCHD3, a novel ATP-dependent chromatin remodeler associated with sites of active transcription. in Molecular and cellular biology 2008
RNA interference identifies CHD4 as an essential gene in regulating breast cancer growth.
Data suggest TCF19 (zeige TCF19 Antikörper) interacts with histone 3 lysine 4 trimethylation through its plant homeodomain finger; TCF19 (zeige TCF19 Antikörper) expression appears to regulate gluconeogenesis in hepatocytes; TCF19 (zeige TCF19 Antikörper) interacts with CHD4 causing NuRD complex recruitment to gene promoters of enzymes involved in gluconeogenesis. (TCF19 (zeige TCF19 Antikörper) = transcription factor 19 (zeige TCF19 Antikörper); CHD4 = chromodomain helicase DNA binding protein 4; NuRD = nucleosome-remodeling-deacetylase)
CHD3 (zeige CHD3 Antikörper) and CHD4 exhibit distinct nuclear localization patterns in unperturbed cells, revealing a subset of specific target genes.
The findings identify that CHD4 deficiency preferentially impairs cell survival via increasing the level of p21 (zeige CDKN1A Antikörper).
Mutation in CHD4 gene is associated with congenital heart defects.
this work identifies CHD4 as an epigenetic coregulator of PAX3 (zeige PAX3 Antikörper)-FOXO1 (zeige FOXO1 Antikörper) activity, providing rational evidence for CHD4 as a potential therapeutic target in alveolar rhabdomyosarcoma.
CHD4 recruits repressive chromatin proteins to sites of DNA damage repair, including DNA methyltransferases where it imposes de novo DNA methylation (zeige HELLS Antikörper). At TSGs, CHD4 retention helps maintain DNA hypermethylation-associated transcriptional silencing.
this study identifies the Chd4-Tbx3 (zeige TBX3 Antikörper) axis in controlling ESC fate and a role of H2A.Z (zeige H2AFZ Antikörper) in maintaining the stability of Chd4 proteins.
report provides evidence for the role of CHD4 in human development and expands an increasingly recognized group of Mendelian disorders involving chromatin remodeling and modification
complex lacking CHD4 that has HDAC (zeige HDAC3 Antikörper) activity can exist as a stable species. The addition of recombinant CHD4 to this nucleosome deacetylase complex reconstitutes a NuRD complex with nucleosome remodeling activity.
Chd4 mutant embryos died before birth and exhibited severe edema, blood-filled lymphatics, and liver hemorrhage. CHD4-deficient embryos developed normal lymphovenous (LV) valves, which regulate the return of lymph to the blood circulation; however, these valves lacked the fibrin-rich thrombi that prevent blood from entering the lymphatic system.
This secreted effector, toxoplasma inhibitor of STAT1 (zeige STAT1 Antikörper)-dependent transcription (TgIST), translocates to the host cell nucleus, where it recruits mouse Mi-2/NuRD to STAT1 (zeige STAT1 Antikörper)-dependent promoters, resulting in altered chromatin and blocked transcription.
this study shows that the chromatin remodeler Mi-2beta controls epidermal homeostasis by regulating the genes involved in keratinocyte and immune-cell activation to maintain an inactive state
preservation of the identity of the two striated (zeige NSDHL Antikörper) muscle types depends on epigenetic repression of the alternate lineage gene program by the chromatin remodeling complex Chd4/NuRD.
CHD4 depletion modulates expression of acute myeloid leukemia (zeige BCL11A Antikörper) cell genes that regulate tumor formation in vivo and colony formation in vitro.
CHD4 allows cells to undertake lineage commitment in vivo by modulating the frequency with which lineage-specification genes are expressed.
Chromatin immunoprecipitation assays showed that CHD4-containing NuRD complexes directly bound the promoters of these genes in endothelial cells
Chd4, interacting with Hdac1 (zeige HDAC1 Antikörper)/2, cooperates with its related proteins Kap1 (zeige TRIM28 Antikörper) and Cbx1 (zeige CBX1 Antikörper) to bind at -207/-148 of the Sox9 (zeige SOX9 Antikörper) promoter.
CHD4 functions as a MAP required for MT stabilization and is involved in generating spindle bipolarity.
The product of this gene belongs to the SNF2/RAD54 helicase family. It represents the main component of the nucleosome remodeling and deacetylase complex and plays an important role in epigenetic transcriptional repression. Patients with dermatomyositis develop antibodies against this protein.
chromodomain helicase DNA binding protein 4
, chromodomain-helicase-DNA-binding protein 4
, ATP-dependent helicase CHD4
, Mi-2 autoantigen 218 kDa protein
, Mi-2 autoantigen
, Mi-2 beta