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anti-Human Filamin A Anticorps:
anti-Mouse (Murine) Filamin A Anticorps:
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Human Monoclonal Filamin A Primary Antibody pour IHC (p), PLA - ABIN560922
Valente, Logan, Mougou-Zerelli, Lee, Silhavy, Brancati, Iannicelli, Travaglini, Romani, Illi, Adams, Szymanska, Mazzotta, Lee, Tolentino, Swistun, Salpietro, Fede, Gabriel, Russ, Cibulskis, Sougnez et al.: Mutations in TMEM216 perturb ciliogenesis and cause Joubert, Meckel and related syndromes. ... dans Nature genetics 2010
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Human Polyclonal Filamin A Primary Antibody pour ICC, IF - ABIN188803
Thoms, Loveridge, Simpson, Clipson, Reinhardt, Dunlop, Stark: Nucleolar targeting of RelA(p65) is regulated by COMMD1-dependent ubiquitination. dans Cancer research 2010
Show all 2 Pubmed References
Human Polyclonal Filamin A Primary Antibody pour IF, IHC - ABIN6711757
Jiao, Deng, Xu, Yu, Li, Yang, Chen, Liu, Huang, Li, Sun: miR-663 induces castration-resistant prostate cancer transformation and predicts clinical recurrence. dans Journal of cellular physiology 2014
a new etiology for macrothrombocytopenia, in which increased RhoA activity is associated with disrupted FLNa/alphaIIbbeta3 interaction.
Septo-optic dysplasia caused by a novel FLNA splice site mutation.
The binding of filamin A by the RtxA11491-1971 domain appears to be a requisite to pak1-mediated MAPK activation, which contributes to the cytoskeletal reorganization and host cell death.
Study identified FLNa as a substrate of NDR2 in vitro and demonstrated that NDR2 phosphorylates FLNa at serine 2152 (S2152) upon TCR-triggering in vivo. NDR2-dependent phosphorylation of FLNa at S2152 releases the binding of this molecule from the inactive conformation of LFA-1, thus allowing the TCR-mediated association of Talin and Kindlin-3 to the cytoplasmatic domain of CD18.
RNA editing of Filamin A pre-mRNA regulates vascular contraction and diastolic blood pressure.
The present findings suggest that calpain1 overexpression predicted a poor outcome in patients with colorectal cancer (CRC)and promoted tumor progression, possibly via FLNA downregulation
Listeria monocytogenes InlB-mediated uptake was accompanied by PKC-alpha-dependent phosphorylation of serine 2152 in FlnA.
Suggest an unanticipated biological function of IRE1alpha in cell migration, whereby filamin A operates as an interphase between the UPR and the actin cytoskeleton.
These two new cases expand the list of live-born FLNA mutation-positive males with connective tissue disease.
Data from this largest series of LOF FLNA mutation patients underscore the importance of serial follow-up to identify and manage these potentially devastating cardiovascular complications.
FLNA overexpression predicts early recurrence of hepatocellular carcinoma after hepatectomy.
Filamin A modulates store-operated calcium entry and then the correct platelet function, by fine-tuning the distribution of STIM1 in the cytoskeleton and the interaction with Orai1 channels.
The authors describe a family with a novel FLNA mutation with a male-expressed, apparently isolated, cardiac phenotype with no skewed X-inactivation pattern in female carriers.
silencing filamin A may inhibit the invasion and migration of breast cancer cells by upregulating 14-3-3sigma.
FLNA overexpression suppressed the proliferation of Bladder Carcinoma cells, blocked cell cycle and promoted apoptosis of Bladder Carcinoma cell.
Silencing filamin A (FLNa) expression in lung cancer cell line A549 cells promoted proliferation, migration, and invasiveness of A549 cells by enhancing the activation of epidermal growth factor receptor and ERK signaling pathway.
The interaction between tissue factor and filamin A is dependent on the differential phosphorylation of Ser253 and Ser258. The interaction with filamin A may translocate cell surface TF to cholesterol-rich lipid rafts, increasing cell surface TF activity as well as TF incorporation and release into microvesicles.
Reduced RNA editing of FLNA gene is associated with psoriasis.
Data indicate mutations in FLNA (Filamin A) associated with Ebstein anomaly.
these observations describe a new mechanism of tissue-specific regulation of FLNA that could reflect the differing mechanical requirements of these cell types during development.
filamin reduces ENaC channel function through direct interaction on the cell surface
Knockdown of filamin A or vimentin in normal cells profoundly suppresses apical extrusion of the neighbouring transformed cells.
Drp1 association with filamin and the actin cytoskeleton contributes to cardiac fragility after myocardial infarct
Study identified FLNa as a substrate of Ndr2 in vitro and demonstrated that Ndr2 phosphorylates FLNa at serine 2152 (S2152) upon TCR-triggering in vivo. Ndr2-dependent phosphorylation of FLNa at S2152 releases the binding of this molecule from the inactive conformation of LFA-1, thus allowing the TCR-mediated association of Talin and Kindlin-3 to the cytoplasmatic domain of CD18.
FlnA and Fmn2 are likely essential to cell proliferation, differentiation and cell death in a variety of tissues and organs, further reiterating the importance of vesicle trafficking in regulation of development
both LRP1 and LDLR expression and agLDL uptake are regulated by P2Y2R in vascular smooth muscle cells, and agLDL uptake due to P2Y2R activation is dependent upon cytoskeletal reorganization mediated by P2Y2R binding to FLN-A
FlnA is a negative regulator of beta2 integrin-dependent cell adhesion and reactive oxygen species production but is required for neutrophil extracellular traps production in primary murine neutrophils
Here the authors report that intermediate progenitor's neuron production is enhanced by abrogating filamin function, leading to the generation of periventricular neurons independent of normal neocortical neurogenesis and neuronal migration.
These results show that FLNA plays crucial roles in asymmetric division during meiotic maturation by regulating ROCK-cofilin-mediated actin reorganization.
FlnA binding to PACSIN2 F-BAR domain regulates membrane tubulation in megakaryocytes and platelets.
FlnA is a critical upstream element of the signaling cascade underlying the myogenic tone.
Bones lacking filamin A are protected from estrogen-mediated post-menopausal osteoporosis
findings suggest a model in which filamin A local translation following axon injury controls localized HDAC5 activity to promote axon regeneration.
Deletion of filamin A in endothelial cells aggravated myocardial infarction-induced left ventricle dysfunction and cardiac failure as a result of defective endothelial response
A new signaling set, phosphatidic acid-S6K1-FLNA-actin, sheds light into the morphogenic pathway of cytoskeletal structures that are crucial for adhesion and cell locomotion during inflammation and metastasis.
Filamin-A is associated with neutrophil uropod retraction.
Analysis of editing in the filamin A encoding mRNA shows very high editing levels outside the nervous system; further shows FLNA editing is mainly achieved by ADAR2 but that in some cases ADAR1 can efficiently compensate for ADAR2.
Filamin a, b-interacting proteins, Cfm1 and Cfm2, are essential for the formation of cartilaginous skeleton.
a major function of FLNa in modulating ion channel abundance and membrane trafficking in neurons, thereby shaping their biophysical properties and function.
FLNA, a large cytoskeletal actin-binding protein, physically interacts with HIF-1alpha and promotes tumor growth and angiogenesis.
The PDZ domain binding motif found in the most C-terminal region of the Sema-1a ICD is necessary for interaction with Vari, but not Cher, indicative of distinct binding modalities. Pbl/Sema-1a-mediated repulsive guidance is potentiated by both vari and cher Genetic analyses further suggest that scaffolding functions of Vari and Cher play an important role in Pbl-mediated Sema-1a reverse signaling.
FLN90, an isoform of the Drosophila ortholog Filamin/cheerio that lacks the actin-binding domain, is here shown to govern the growth of postsynaptic membrane folds and the composition of glutamate receptor clusters at the larval neuromuscular junction.
Here we show using Drosophila indirect flight muscle that the filamin ortholog Cheerio in conjunction with the giant elastic protein titin plays a crucial role in keeping thin filaments stably anchored at the Z-disc. We identify the filamin domains required for interaction with the titin ortholog Sallimus, and we demonstrate a genetic interaction of filamin with titin and actin.
study identifies Cher as a new target of JNK signaling that links cytoskeleton dynamics to tumor progression.
Data indicate that during embryonic development, the expression of Filamin and Ten-m partially overlap in ectodermal cells.
Filamin is required for ovarian follicle cell motility during oogenesis.
The protein encoded by this gene is an actin-binding protein that crosslinks actin filaments and links actin filaments to membrane glycoproteins. The encoded protein is involved in remodeling the cytoskeleton to effect changes in cell shape and migration. This protein interacts with integrins, transmembrane receptor complexes, and second messengers. Defects in this gene are a cause of several syndromes, including periventricular nodular heterotopias (PVNH1, PVNH4), otopalatodigital syndromes (OPD1, OPD2), frontometaphyseal dysplasia (FMD), Melnick-Needles syndrome (MNS), and X-linked congenital idiopathic intestinal pseudoobstruction (CIIPX). Two transcript variants encoding different isoforms have been found for this gene.
actin binding protein 280
, endothelial actin-binding protein
, non-muscle filamin
, filamin A, alpha (actin binding protein 280)
, GENA 379
, actin-binding protein 280
, dilated pupils 2
, filamin A
, Endothelial actin-binding protein 280)
, filamin, alpha
, filamin A, alpha
, filamin B
, filamin isoform B
, shi kong
, 450 kDa protein