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Human Polyclonal KAT5 Primary Antibody für ELISA, WB - ABIN543210
Legube, Linares, Tyteca, Caron, Scheffner, Chevillard-Briet, Trouche: Role of the histone acetyl transferase Tip60 in the p53 pathway. in The Journal of biological chemistry 2004
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Human Polyclonal KAT5 Primary Antibody für ELISA, WB - ABIN543209
Patel, Du, Ard, Phillips, Carella, Chen, Rakowski, Chatterjee, Lieberman, Lane, Blobel, McMahon: The c-MYC oncoprotein is a substrate of the acetyltransferases hGCN5/PCAF and TIP60. in Molecular and cellular biology 2004
Show all 3 Pubmed References
Human Monoclonal KAT5 Primary Antibody für IHC, ELISA - ABIN1724672
Jin, Cai, Li, Conaway, Workman, Conaway, Kusch: In and out: histone variant exchange in chromatin. in Trends in biochemical sciences 2005
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Human Polyclonal KAT5 Primary Antibody für WB - ABIN6682286
Mao, Sun: Arabidopsis seed-specific vacuolar aquaporins are involved in maintaining seed longevity under the control of ABSCISIC ACID INSENSITIVE 3. in Journal of experimental botany 2015
Human Polyclonal KAT5 Primary Antibody für ICC, IF - ABIN4359851
Laurberg, Brems-Eskildsen, Nordentoft, Fristrup, Schepeler, Ulhøi, Agerbaek, Hartmann, Bertz, Wittlinger, Fietkau, Rödel, Borre, Jensen, Orntoft, Dyrskjøt: Expression of TIP60 (tat-interactive protein) and MRE11 (meiotic recombination 11 homolog) predict treatment-specific outcome of localised invasive bladder cancer. in BJU international 2013
Human Polyclonal KAT5 Primary Antibody für IHC, IHC (p) - ABIN4359852
Zaini, Müller, de Jong, Ackermann, Hartleben, Kortman, Gührs, Fusetti, Krämer, Guryev, Calkhoven: A p300 and SIRT1 Regulated Acetylation Switch of C/EBPα Controls Mitochondrial Function. in Cell reports 2018
Human Polyclonal KAT5 Primary Antibody für IHC (p), SimWes - ABIN4359854
Krukenberg, Jiang, Steen, Mitchison: Basal activity of a PARP1-NuA4 complex varies dramatically across cancer cell lines. in Cell reports 2014
Results indicate that Tip60 complex coordinates cell cycle progression and expression of bgcn to help drive GSC daughters toward a differentiation program.
findings reveal an evolutionarily conserved functional link between Myc, the Tip60 complex, and the molecular network controlling cell polarity and asymmetric cell division.
most HIF1A targets require either TIP60, the CDK8-Mediator complex, or both as coactivators for full expression in hypoxia.
Our results implicate Tip60 as a critical mediator of EE-induced benefits, and provide broad insights into synergistic behavioral and epigenetic based therapeutic approaches for treatment of cognitive disorder.
compromising Tip60 histone acetyltransferase activity in the CySC lineage recapitulates loss-of-function phenotypes of E(Pc), suggesting that Tip60 and E(Pc) act together, consistent with published biochemical data.
critical for morphology and function of the mushroom body
Heat Shock Factor recruits the dTip60 complex to the hsp70 loci in cells treated with salicylate, which triggers chromatin remodeling at these loci without transcription activation.
Excess Tip60 exerts a neuroprotective role in axonal transport and functional locomotion defects in an animal model of Alzheimer's disease.
a novel mechanism for Tip60 mediated sleep-wake regulation via control of axonal growth and PDF levels within the small ventrolateral neurons-encompassing neural network
a functional interaction between Tip60 and APP in mediating nervous system development and apoptotic neuronal cell death
The role of Tip60 HAT activity in transcriptional control during multicellular development in vivo, was investigated.
Ubiquitous dTip60 knock-down in flies was lethal, whereas knock-down in the wing imaginal disk led to developmental defects.
demonstrated that the dTip60 chromatin-remodeling complex acetylates nucleosomal phospho-H2Av and exchanges it with an unmodified H2Av; both the histone acetyltransferase dTip60 and the atpase Domino/p400 catalyze the exchange of phospho-H2Av
TIP60 complex can promote the generation of silent chromatin.
TIP60 is differentially expressed during Drosophila development, with transcript levels significantly peaking during embryogenesis, and is essential for multicellular development.
A unique mechanism of Endogenous retroviral elements regulation in cancer cells mediated by TIP60 and BRD4 through regulation of histone H3 K9 trimethylation.
these findings suggest that Tip60-ATM signaling has a functional contribution to the recruitment of TMPK to DNA damage sites, thereby increasing local dTTP synthesis for DNA repair.
mTORC1 and GSK3-TIP60 signaling converge to modulate autophagosome maturation and lipid metabolism through Pacer.
Tip60 mediates acetylation at lysine residues of SPZ1 at positions 369 and 374, and of TWIST1 at positions 73 and 76, which are required for SPZ1-TWIST1 complex formation and cancer cell migration in vitro and in vivo. Ectopic SPZ1 and TWIST1 expression, but not that of TWIST1 alone, enhanced VEGF expression via the recruitment of BRD4, enhancing RNA-Pol II-dependent transcription and inducing metastasis.
Tat-interactive protein 60 (Tip60) is one of the subtypes of histone-acetyltransferase. It is reported that antigen stimulation leads to the increase in expression of Tip60.
Overexpression of TIP60 inhibited viral protein and RNA expression and reduced the progeny viral titer. Further study revealed that TIP60 inhibited Influenza A virus replication through activation of TBK1-IRF3 signaling pathway.
Analysis of the apo-structure reveals a putative peptide-binding site that might be occluded by the basic side chain of a residue in a unique beta hairpin between the two N-terminal strands of the beta barrel, leading to the inability of TIP60-CB to bind histones.
our data indicate that, during transcription, phosphorylation of TIP60 at two sites has different regulatory effects on TIP60, whereby S90 phosphorylation controls association with the transcription machinery, and S86 phosphorylation is regulating TIP60 HAT activity.
our results suggest that TIP60 promotes the expression of FA and HR genes that are important for ICL repair and the chemoresistant phenotype under chronic treatment with cisplatin.
Results show that KAT5 expression is decreased in prostate cancer (PCa) and correlated with shorter recurrence-free survival.
Tip60 suppressed growth and metastasis throughout the progression of cholangiocarcinoma and identified the PI3K/AKT pathway as a dominant signal of Tip60.
TIP60 is involved in several adipogenesis mechanisms through its interaction with three important proteins: PPARc, USP7, and GPR50. These actors act also in different processes of breast cancer development.
These findings demonstrate the critical regulation of TIP60/p53 pathway in apoptosis upon metabolic stress and provide a novel insight into the down-regulation of TIP60 in tumor cells.
Our data demonstrate for the first time that TIP60 through its MYST domain directly interacts with UHRF1
These results suggest that TIP60, in concert with other cellular factors, plays an important role in the regulation of the HBV chromatin structure by acting as a critical component of the intrinsic antiviral defense, which sheds new light on the regulation of HBV replication.
Irreversible inhibition of USP7 results in durable downstream biological responses in cells, including down-regulation of Tip60 and consequent impairment of Treg suppressive function
NOTCH1 inhibits activation of ATM by impairing the formation of an ATM-FOXO3a-KAT5 complex.
Collectively, the data establish a hitherto unknown liaison among MDR1, BMI1 and TIP60 and provide mechanistic insights into cisplatin-induced MDR1 expression resulting in acquired cross-resistance against paclitaxel, doxorubicin and likely other anticancer drugs.
TIP60-mediated growth suppression of HPV-induced cervical cancer is mediated in part due to TERT repression through Sp1 acetylation. In summary, our study has identified a novel substrate for TIP60 catalytic activity and a unique repressive mechanism acting at the TERT promoter in virus-induced malignancies.
Nrf1, RUVBL1, and TIP60 proteins were co-recruited to the promoter regions of proteasome genes after proteasome inhibitor treatments.
Study in mice reports that Marcks is regulated by acetylation through Tip60 and Sirt2. Maternal diabetes-induced MARCKS acetylation is required for its phosphorylation, which disables the protective effects of MARCKS on mitochondria and the endoplasmic reticulum, leading to cellular organelle stress and neural tube defect formation.
Fatty acids stimulate Tip60-dependent acetylation and endoplasmic reticulum translocation of phosphatidic acid phosphatase lipin 1 to generate diacylglycerol for triacylglycerols synthesis.
Tip60 controls homologous recombination (HR)-directed DNA repair, and that Tip60 levels correlate inversely with a gene expression signature associated with defective HR-directed DNA repair.
Results report that EPC1 and TIP60 are co-expressed in male germ cells. Genetic ablation of either Epc1 or Tip60 disrupts hyperacetylation and impairs histone replacement, in turn causing aberrant spermatid development.
these results identify a new compaction pathway of mammalian pericentric heterochromatin relying on Tip60 that might be dependent on BRD2 recruitment by H4K12 acetylation.
The expression of putative SOX4 target genes during myoblast differentiation is specifically regulated by the molecular switching of the co-activator KAT5 and the co-repressor HDAC1 on SOX4 transcriptional activation.
TIP60 K327 acetylation allows TIP60 to switch binding partners. conditional knockout in Treg cells results in autoimmune disease.
Allele compensation in tip60+/- mice rescues white adipose tissue function in vivo.
Tip60 hyperacetylates histone H4 in Ras-transformed cells.Tip60 coordinates histone acetylation at both local and global levels to facilitate Ras-induced transformation.
RGS6 suppresses Ras-induced cellular transformation by facilitating Tip60-mediated Dnmt1 degradation and promoting apoptosis
Early adipogenesis is regulated through USP7-mediated deubiquitination of the histone acetyltransferase TIP60.
SLX2 interacts with synaptonemal complex central element protein 2 (SYCE2) and histone acetyltransferase TIP60.
these results suggest that Tip60 binds with Pax6 and that this physical interaction leads to the full-transcriptional activation of Pax6 during retina development.
Tip60 may function in a tumor suppressor pathway(s) to maintain adult cardiomyocytes in replicative senescence.
found that Nrl activated rhodopsin and Ppp2r5c transcription by recruiting Tip60 to promote histone H3/H4 acetylation
Data demonstrate that GPR50 can enhance TIP60-coactiavtion of glucocorticoid receptor (GR) signalling.
Partial Tip60 loss increased Rora and Rora-mediated gene expression and delayed ATXN1-mediated cerebellar degeneration during mid-stage disease progression.
Tip60-dependent recruitment of RNR plays an essential role in dNTP supply for DNA repair
The protein encoded by this gene belongs to the MYST family of histone acetyl transferases (HATs) and was originally isolated as an HIV-1 TAT-interactive protein. HATs play important roles in regulating chromatin remodeling, transcription and other nuclear processes by acetylating histone and nonhistone proteins. This protein is a histone acetylase that has a role in DNA repair and apoptosis and is thought to play an important role in signal transduction. Alternative splicing of this gene results in multiple transcript variants.
K(lysine) acetyltransferase 5
, Tat-interactive protein
, histone acetyltransferase Tip60
, HIV-1 tat interactive protein
, 60 kDa Tat-interactive protein
, HIV-1 Tat interactive protein, 60kDa
, K-acetyltransferase 5
, Tat interacting protein, 60kDa
, cPLA(2)-interacting protein
, cPLA2 interacting protein
, histone acetyltransferase HTATIP
, histone acetyltransferase KAT5
, HIV-1 tat interactive protein 1, 60 kDa homolog
, HIV-1 tat interactive protein 1, homolog
, Tat-interactive protein-60
, lysine acetyltransferase 5
, HIV-1 Tat interacting protein, 60kDa
, HIV-1 Tat interactive protein 60 kD
, HIV-1 Tat interactive protein, 60 kD
, HIV-1 tat interactive protein, homolog
, Histone acetyltransferase HTATIP