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anti-Human beta Actin Antikörper:
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Human Monoclonal beta Actin Primary Antibody für IHC (p), WB - ABIN3044484
Pan, Quan, Liu, Xu, Zhu, Huang, Tian: Epigallocatechin gallate reverses cTnI-low expression-induced age-related heart diastolic dysfunction through histone acetylation modification. in Journal of cellular and molecular medicine 2017
Show all 453 Pubmed References
Cat (Feline) Monoclonal beta Actin Primary Antibody für ELISA, FACS - ABIN153386
Dietz, Souan, Knutson, Bulur, Litzow, Vuk-Pavlovic: Imatinib mesylate inhibits T-cell proliferation in vitro and delayed-type hypersensitivity in vivo. in Blood 2004
Show all 349 Pubmed References
Cow (Bovine) Polyclonal beta Actin Primary Antibody für IF (cc), WB - ABIN724340
Li, Zhou, Guo, Wang: Polypeptide from Chlamys farreri inhibits UVB-induced HaCaT cells apoptosis via inhibition CD95 pathway and reactive oxygen species. in Free radical research 2008
Show all 181 Pubmed References
Human Polyclonal beta Actin Primary Antibody für WB - ABIN3044573
Chang, Zhang, Lihua, Feng: T3 inhibits the calcification of vascular smooth muscle cells and the potential mechanism. in American journal of translational research 2016
Show all 131 Pubmed References
Bird (Avian) Polyclonal beta Actin Primary Antibody für BP, EIA - ABIN153388
Adler, Huang, Wolin, Kaminski: Oxidant stress leads to impaired regulation of renal cortical oxygen consumption by nitric oxide in the aging kidney. in Journal of the American Society of Nephrology : JASN 2003
Show all 93 Pubmed References
Human Monoclonal beta Actin Primary Antibody für WB - ABIN6671957
Pan, Wang, Zhang, Zhang, Zhang, Wang, Xu, Zhang, Hu, Zhang, Du, Wang: Hypoxia-induced microRNA-191 contributes to hepatic ischemia/reperfusion injury through the ZONAB/Cyclin D1 axis. in Cell death and differentiation 2019
Show all 67 Pubmed References
Mouse (Murine) Monoclonal beta Actin Primary Antibody für WB - ABIN3020544
Yang, Hu, Fan, Zhang, Zhong, Guo, Qin, Chen: Picornavirus 2A protease regulates stress granule formation to facilitate viral translation. in PLoS pathogens 2018
Show all 67 Pubmed References
Human Polyclonal beta Actin Primary Antibody für IHC, IHC (p) - ABIN4284408
Morita, Motoyama, Kitayama, Morioka, Kifune, Dohi: Spinal antiallodynia action of glycine transporter inhibitors in neuropathic pain models in mice. in The Journal of pharmacology and experimental therapeutics 2008
Show all 58 Pubmed References
Human Polyclonal beta Actin Primary Antibody für IHC, SimWes - ABIN153417
Watters, Kraja, Meucci, Province, McLeod: Genome-wide discovery of loci influencing chemotherapy cytotoxicity. in Proceedings of the National Academy of Sciences of the United States of America 2004
Show all 40 Pubmed References
Human Polyclonal beta Actin Primary Antibody für WB - ABIN6710112
Liu, Chen, Li, Hu, Liu, Tian, Zhao, Wu, Zhou, Qiao: Interaction between cyclooxygenase-2, Snail, and E-cadherin in gastric cancer cells. in World journal of gastroenterology 2014
Show all 38 Pubmed References
Recurrent ACTB-FOSB fusions are found in pseudomyogenic hemangioendothelioma.
the present study uncovered a yet unrecognized nuclear coupling of AKT and provides insights into the involvement of AKT in the interaction network of nuclear actin.
Report recurrent GLI1-ACTB gene fusions in a group of malignant mesenchymal neoplasms involving soft tissue, and occasionally bone, with an often nested epithelioid phenotype and strong S100 immunoreactivity.
All tested genes may be recommended as universal reference genes for data normalization in gene expression studies under different treatment regimens both in primary glioblastomas and astrocytomas of different grades (World Health Organization grades II-IV), respectively. In summary, ACTB and SDHA exhibited the best stability values and showed the lowest intergroup expression variability.
During cell adhesion, an active multistage process naturally leads to pattern transitions from actin vortices over stars into asters.
Haploinsufficiency of ACTB is the main cause of the clinical phenotype observed in the patients with 7p22.1 microdeletions.
Baraitser-Winter cerebrofrontofacial syndrome is caused by missense mutations in the cytoplasmic beta- and gamma-actin genes ACTB and ACTG1. We provide an overview of the clinical characteristics (including some novel findings in four recently diagnosed patients), diagnosis, management, mutation spectrum and genetic counselling.
The authors describe heterozygous ACTB deletions and nonsense and frameshift mutations in 33 individuals with developmental delay, apparent intellectual disability, increased frequency of internal organ malformations (including those of the heart and the renal tract), growth retardation, and a recognizable facial gestalt.
Data indicate AIM1 (absent in melanoma 1) as an actin binding protein and show that it regulates cytoskeletal remodeling and cell migration in prostate epithelial cells.
Case Report: gastric pericytoma harboring the exceptionally rare translocation t(7;12) resulting in ACTB-GLI1 gene fusion.
Data suggest that, in T-lymphocytes, nitric oxide generated by eNOS S-nitrosylates Cys374 on ACTB and thus regulates activation/recruitment of PRKCQ at immune synapse; S-nitrosylation of beta-actin impairs actin binding to PFN1 and regulates protein transport in lamellipodia. (eNOS = nitric oxide synthase 3; ACTB = beta-actin; PRKCQ = protein kinase C-theta; PFN1 = profilin-1)
Data indicate that the IQGAP1 N-terminal fragment spanning residues 1-191 (CHDF) binds to both F-actin and Ca(2+)/calmodulin.
Based on present and published dup7p22.1 patients we suggest that renal abnormalities might be an additional feature of the 7p22.1 microduplication syndrome.We also pinpoint the ACTB gene as the key gene affecting the 7p22.1 duplication syndrome phenotype.
We suggest that haploinsufficiency of ACTB may be responsible for the clinical features of patients with 7p22.1 microdeletions
crucial role of Glu270 in ADP-ribosylation of actin by Ia
Studies indicate that the process of megakaryocyte maturation and the formation of proplatelets are essential steps in the production of mature platelets and both depend heavily on the actin and microtubule cytoskeletons.
Data show that tripartite motif-containing 28 protein (TRIM28) and beta-actin were up-regulated in the glioblastoma multiforme (GBM) stem-like cells compared to the controls.
Data suggest that by binding to both clathrin and F-actin, mammalian actin-binding protein 1 (mAbp1; HIP-55 or SH3P7) is specifically recruited at a late stage of clathrin-coated pits (CCPs) formation, which subsequently recruits dynamin to CCPs.
The results indicate that the disease-related human beta-actin mutations p.R183W and p.E364K affect interdomain mobility and nucleotide interactions as a basis for the formation of disease phenotypes in patients.
Data indicate the WASp-interacting protein (WIP)-Wiskott-Aldrich syndrome protein (WASp) interaction in the regulation of actin-dependent processes.
In beta-actin null cells, we show evidence that the enhanced TGF-b signaling relies on the active utilization of latent TGF-b1 in the cell culture medium. TGF-b signaling activation contributes to the elevated reactive oxygen species production, which is likely mediated by the upregulation of Nox4.
our work reveals fundamental differences in the role of the cortical beta-actin cytoskeleton in mature muscle compared with cell culture
Data, including data from studies using knockout mice, suggest that Actb and Actg1 are enriched in isolated membrane preparations from skeletal muscle which represent interface between mitochondria and sarco-endoplasmic reticulum; these structures appear to be important in signaling, mitochondrial dynamics, and muscle relaxation. (Actb = beta actin cytoplasmic 1; Actg1 = actin gamma cytoplasmic 1)
Essential nucleotide- and protein-dependent functions of Actb/beta-actin.
These results suggest a a novel genome-wide mechanism where the polymerase-associated beta-actin synergizes with NM1 to coordinate permissive chromatin with Pol I transcription, cell growth, and proliferation.
Two actin isoforms, beta- and gamma-actin, are crucial for slow, rapid, bulk, and overshoot endocytosis at large calyx-type synapses, and for slow endocytosis and bulk endocytosis at small hippocampal synapses.
Melatonin treatment for 1 h increased monomeric actin and decreased polymeric actin.
Disruption of the in vivo interaction of KIF11 with ZBP1 delocalizes beta-actin mRNA and affects cell migration.
TIA proteins can function as long-term regulators of the ACTB mRNA metabolism in mouse and human cells.
Actin binding proteins associated with stress fiber or focal adhesion formation are overexpressed in the beta-actin knock-out cells and many of these contain CH-, LIM- or EFh- domains.
Absence of beta-actin severely hampers formation of the peripheral nervous system, due to defective neural crest migration.
Data indicate that ectopic phosphatidylinositol 3,4,5-triphosphate (PIP3) elevation alone activated membranes to form actin-based structures whose behavior was similar to that of growth-cone-like "waves".
this work demonstrated that dendritic beta-actin messenger RNA and ribosomes are in a masked, neuron-specific form.
chorein interacts with beta-adducin and beta-actin.
RNA polymerase II, glyceraldehyde-3-phosphate dehydrogenase (Gapdh), and hypoxanthine phophoribosyltransferase (Hprt) show a more stable gene expression as candidate genes than do ribosomal 18s and Actb.
The findings suggested that local translation of beta-actin in growth cones of motoneurons is regulated by laminin signalling and that this signalling is disturbed in survival of motoneuron protein-deficient motoneurons.
Data suggest that in beta-actin knockout cells other actins compensate for beta-actin in cell migration process.
Data indicate that Ubc and Ywhaz were best correlated for B cells and lymphocytes, whereas Ubc and Gapdh were the best combination for non-B cells, and Actb and Hprt1 were the least stably expressed genes for B cells and non-B cell.
the zipcode-binding protein 1 transports beta-actin mRNA to the focal adhesion compartment, it dwells for minutes, associating its localization with motility through the formation of stable connections between adhesions and newly synthesized actin filaments
These data show that thymosinbeta4 and beta-actin are over-expressed during nurse cell formation upon T. spiralis infection and may be involved in nurse cell formation along with other actin-binding proteins.
The disruption of DNlg1, DNlg2, or their presynaptic partner neurexin (DNrx) led to a dramatic decrease in the amount of F-actin. Further study showed that DNlg1, but not DNlg2 or DNlg3, directly interacts with the WRC via its C-terminal interacting receptor sequence.
These findings revise the existing spermiation model in Drosophila and suggest that somatic cells can actively oppose mechanical cell invasion attempts using calibrated F-actin dynamics in situ
Data suggest that the molecular and structural mechanism of actin polymerization by Spire should apply to other actin-binding proteins that contain WH2 domains in tandem.
actin filament subunits were directly modified by Mical on their conserved pointed-end, critical for filament assembly; Mical posttranslationally oxidized the methionine 44 residue within D-loop of actin, severing filaments and decreasing polymerization
essential cytoplasmic actin isoform
A mutational strategy is used to express monomeric 5C actin that is incapable of polymerization, able to bind skeletal myosin subfragment 1 and form a homogeneous complex, an ideal candidate for structural studies of actin complexes with motor proteins.
Taken together, these data can be explained by a model that associates components of the secretory machinery to the F-actin cortex through flexible links
biophysical analysis reveals that the open nucleotide pocket of the profilin/actin x-ray structure is unstable and closes in the absence of profilin
determination of the crystal structure of oxidized beta-actin to a resolution of 2.6 A; identification of oxidation of cysteine 272 in the crystallized actin dimer
This study showed that beta-actin, L32 ribosomal protein, and ATP5B proteins were the most stabily expressed genes in cryopreserved horse semen.
HnRNP-R-mediated axonal beta-actin mRNA translocation plays an essential physiological role for axon growth and presynaptic differentiation.
Data show that shortly after anaphase onset oocytes and embryonic cells exhibit cortical waves of Rho activity and F-actin polymerization.
This gene encodes one of six different actin proteins. Actins are highly conserved proteins that are involved in cell motility, structure, and integrity. This actin is a major constituent of the contractile apparatus and one of the two nonmuscle cytoskeletal actins.
PS1TP5-binding protein 1
, actin, cytoplasmic 1
, beta cytoskeletal actin
, actin, alpha 1, skeletal muscle
, A-X actin-like protein
, actin, beta, cytoplasmic
, melanoma X-actin
, cytoplasmic beta-actin
, actin beta
, 5C actin
, actin 5 C
, actin 5C
, actin 5c
, actin A1
, cellular cytoskeletal beta-actin
, cytoplasmic 1
, cytoskeletal beta actin
, gamma non-muscle actin
, beta actin
, actin, beta
, Actin, cytoplasmic 1
, Beta-actin A
, beta actin1