Fermitin Family Member 3 (FERMT3) ELISA Kits

Mouse (Murine) Fermitin Family Member 3 (FERMT3) interaction partners

1. these results demonstrate that kindlin-3 in neutrophils is involved in modulating reactive oxygen species and extracellular trap signaling

2. FERMT3 (kindlin-2) role in proline synthesis and tumor growth.Kindlin-2 regulates proline synthesis through PYCR1.

3. kindlin-3 is dispensable for integrin-mediated T cell progenitor adhesion and signalling at low and indispensable at high shear forces.

4. expression is markedly suppressed in pathologically activated osteoclasts

5. Structure and lipid-binding properties of the kindlin-3 pleckstrin homology domain has been reported.

6. 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.

7. 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.

8. Optimal T cell activation and B cell antibody responses in vivo require the interaction between Integrin beta2 and kindlin-3.

9. 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.

10. ADAP interacts with talin and kindlin-3 to promote platelet Integrin alphaIIbbeta3 activation and stable fibrinogen binding.

11. 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.

12. 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.

13. 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

14. Kindlin-3 is central to conversion of mechanical force to intracellular signaling via calcium influx.

15. Data indicate that Kindlin-3 specifically recognizes the integrin membrane-distal tail NPXY motif in both the beta(1A) and beta(1D) isoforms.

16. Both talin-1 and kindlin-3 are required for induction of the high-affinity conformation of LFA-1 with an open headpiece, which results in neutrophil arrest.

17. We investigated the role of talin-1, kindlin-3, and alpha-actinin-1 in the upregulation of alpha(4)beta(1) integrin affinity and consequent inflammatory leukocyte adhesive events

18. Osteoclasts require their entire integrin repertoire to be regulated by kindlin-3 to orchestrate bone homeostasis.

19. The genomic organization, gene expression and subcellular localization of murine Kindlins-1 to -3, is described.

20. Kindlin-3 was identified as a novel and essential element for platelet integrin activation in hemostasis and thrombosis.

Xenopus laevis Fermitin Family Member 3 (FERMT3) interaction partners

1. Kindlin3 morphant phenotypes included defects in epidermal ciliary beating and partial paralysis at tailbud stages but these embryos recovered eventually as morpholino levels decayed.

Human Fermitin Family Member 3 (FERMT3) interaction partners

1. these results demonstrate that kindlin-3 in neutrophils is involved in modulating reactive oxygen species and extracellular trap signaling

2. FERMT3 (kindlin-2) role in proline synthesis and tumor growth.Kindlin-2 binds PYCR1 and PYCR2 proteins.

3. In patients with dysfunctions of ORAI1, STIM1 or FERMT3, severe immunodeficiency is frequently linked to abnormal platelet activity. Measurement of thrombus formation at low shear rate confirmed a greater impairment of platelet functionality in the ORAI1 patients than in the STIM1 patient. For 3 patients/relatives with a FERMT3 mutation, all parameters of thrombus formation were strongly reduced.

4. FERMT3 regulates glioma cell activity through integrin-mediated Wnt/beta-catenin signaling.

5. Expression of Kindlin2 is associated with tumor grade.

6. 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

7. kindlin-3 plays an important role in maintaining a proper conformation of the resting alpha4beta1 to mediate both rolling and firm cell adhesion

8. Kindlin-3 regulates c-Myc protein expression in the human chronic myeloid leukemia cell line K562.

9. 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.

10. Suppression of the Kindlin-2-integrin beta1-AKT regulatory axis is an alternative mechanism underlying the tumor suppressor function of miR-200b in esophageal squamous cell carcinoma.

11. Kindlin-3/FERMT3 is upregulated in atherosclerotic, mainly in cells of monocytic origin and of M2 type. Simultaneous upregulation of ITGB2 suggests a synergistic effect on leukocyte adherence and transmigration into the vessel wall.

12. 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.

13. A new C>T point mutation was found in exon 13 in the FERMT3 gene in an infant diagnosed with LAD-III. KINDLIN-3 expression is required for platelet aggregation and leukocyte function, but also osteoclast-mediated bone resorption.

14. Mig-2 significantly attenuates the antitumor action of cisplatin.

15. The data uncover a novel and unexpected tumor suppressor role of Kindlin-3 which can influence integrins targeted therapies development.

16. High Kindlin-2 expression promotes pancreatic ductal adenocarcinoma progression.

17. These data identify a role of kindlin-3 phosphorylation in integrin b3 activation and provide a basis for functional differences between kindlin-3 and the two other kindlin paralogs.

18. Kindlin 2 expression was significantly increased in luteinized granulosa cells from patients with polycystic ovary syndrome.

19. kindlin-2 tyrosine phosphorylation and interaction with Src serve as a regulatable switch downstream of focal adhesion kinase in the integrin outside-in signaling circuit controlling cell migration and proliferation

20. Direct activation of RhoA with recombinant bacterial cytotoxic necrotizing factor y reverted the abnormal phenotype and barrier function of kindlin-2-deficient keratinocytes and skin equivalents.