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Kindlins are a small family of proteins that mediate protein-protein interactions involved in integrin activation and thereby have a role in cell adhesion, migration, differentiation, and proliferation. Zusätzlich bieten wir Ihnen FERMT3 Kits (9) und FERMT3 Proteine (3) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 75 products:
Human Polyclonal FERMT3 Primary Antibody für IF, WB - ABIN529478
Feng, Li, Yau, Lee, Tang, Xue, Zhou, Lim, Cornvik, Ruedl, Shochat, Tan: Kindlin-3 mediates integrin ?L?2 outside-in signaling, and it interacts with scaffold protein receptor for activated-C kinase 1 (RACK1). in The Journal of biological chemistry 2012
Human Polyclonal FERMT3 Primary Antibody für ELISA, WB - ABIN4311346
Svensson, Howarth, McDowall, Patzak, Evans, Ussar, Moser, Metin, Fried, Tomlinson, Hogg: Leukocyte adhesion deficiency-III is caused by mutations in KINDLIN3 affecting integrin activation. in Nature medicine 2009
Structure and lipid-binding properties of the kindlin-3 pleckstrin (zeige PLEK Antikörper) homology domain has been reported.
Mice expressing as little as 5% of kindlin-3 were viable and protected from spontaneous bleeding and infections. In vitro platelet functions, leukocyte adhesion, extravasation, and bacterial clearance were diminished. Bleeding time increased.
The accumulation of HSPCs in the circulation of leukocyte adhesion deficiency type III patients, who lack Kindlin-3, underlines the conserved functions of Kindlin-3 in man and the importance of our findings for human disease.
Optimal T cell activation and B cell antibody responses in vivo require the interaction between Integrin beta2 and kindlin-3.
Direct binding of kindlin-3 to integrin alphaIIbbeta3 is involved in supporting integrin alphaIIbbeta3 activation and integrin alphaIIbbeta3-dependent responses of platelets and consequently contributes significantly to arterial thrombus formation.
ADAP interacts with talin and kindlin-3 to promote platelet Integrin alphaIIbbeta3 activation and stable fibrinogen binding.
the requirement of Kindlin-3 for effector T cells to induce alpha4beta1 and alphaLbeta2 integrin ligand binding and stabilization of integrin-ligand bonds is critical when integrin ligand levels are low, but of less importance when integrin ligand levels are high.
This is the first in vivo demonstration that Kindlin-3-stabilized integrin adhesions, although essential for lymphocyte arrest on blood vessels and interstitial motility, are not obligatory for leukocyte diapedesis.
the beta-2-integrin-kindlin-3 interaction is particularly important in adhesion strengthening under shear flow, and for T-cell homing to lymph nodes, but dispensable for T cell activation which occurs in a shear-free environment
Kindlin-3 is central to conversion of mechanical force to intracellular signaling via calcium influx.
FERMT3 regulates glioma cell activity through integrin-mediated Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling.
this case report describes a female Thai patient who was diagnosed with leukocyte adhesion deficiency type III with a novel mutation in FERMT3, presenting with a humoral immune defect
kindlin-3 plays an important role in maintaining a proper conformation of the resting alpha4beta1 to mediate both rolling and firm cell adhesion
Kindlin-3 regulates c-Myc (zeige MYC Antikörper) protein expression in the human chronic myeloid leukemia (zeige BCL11A Antikörper) cell line K562.
NMR studies demonstrated that the F1 loop of kindlin-3 is globally unfolded but stretches of residues assuming transient helical conformations could be detected in aqueous solution.
Suppression of the Kindlin-2 (zeige FERMT2 Antikörper)-integrin beta1-AKT (zeige AKT1 Antikörper) regulatory axis is an alternative mechanism underlying the tumor suppressor function of miR (zeige MLXIP Antikörper)-200b in esophageal squamous cell carcinoma.
Kindlin-3/FERMT3 is upregulated in atherosclerotic, mainly in cells of monocytic origin and of M2 type. Simultaneous upregulation of ITGB2 (zeige ITGB2 Antikörper) suggests a synergistic effect on leukocyte adherence and transmigration into the vessel wall.
A new C>T point mutation was found in exon 13 in the FERMT3 gene in an infant diagnosed with LAD (zeige DLD Antikörper)-III. KINDLIN-3 expression is required for platelet aggregation and leukocyte function, but also osteoclast-mediated bone resorption.
Mig-2 (zeige FERMT2 Antikörper) significantly attenuates the antitumor action of cisplatin.
Kindlins are a small family of proteins that mediate protein-protein interactions involved in integrin activation and thereby have a role in cell adhesion, migration, differentiation, and proliferation. The protein encoded by this gene has a key role in the regulation of hemostasis and thrombosis. This protein may also help maintain the membrane skeleton of erythrocytes. Mutations in this gene cause the autosomal recessive leukocyte adhesion deficiency syndrome-III (LAD-III). Alternative splicing results in multiple transcript variants encoding distinct isoforms.
fermitin family homolog 3
, unc-112-related protein 2
, fermitin family member 3
, MIG2-like protein
, UNC-112 related protein 2
, kindlin 3