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FERMT1 encodes a member of the fermitin family, and contains a FERM domain and a pleckstrin homology domain. Additionally we are shipping FERMT1 Antibodies (49) and FERMT1 Proteins (5) and many more products for this protein.
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The rof/kindlin-1 mutant zebrafish provi (show ILK ELISA Kits)des a unique model system to study epidermal adhesion mechanisms in vivo.
these data define a novel role for Kin1 in microtubule acetylation and stability
These results indicate that Kindlin-1 is essential in EGF (show EGF ELISA Kits)-induced re-epithelialization in skin wound healing and provide additional rationale for the clinical application of EGF (show EGF ELISA Kits) in the treatment of acute wounds.
By modulating its affinity with kindlin, beta3 integrin (show ITGB3 ELISA Kits) may be able to locate near the cell edge where it can control beta1 integrin activation and clustering.
Kindlin-1 is highly expressed in epithelial tissues derived from ectoderm and endoderm. Kindlin-1 was als (show FERMT2 ELISA Kits)o found highly expressed in endoderm/ectoderm-derived tissues in embryos.
Kindlin-1 controls keratinocyte adhesion through beta1-class integrins and proliferation and differentiation of cutaneous epithelial stem cells via TGF-beta (show TGFB1 ELISA Kits) activation and Wnt (show WNT2 ELISA Kits)-beta-catenin (show CTNNB1 ELISA Kits) signal inhibition.
Kindlin-1 and Kindlin-2 (show FERMT2 ELISA Kits) have opposite roles in lung cancers
Kindlin-1 in mice gives rise to skin atrophy and an intestinal epithelial dysfunction with similarities to human ulcerative colitis.
Kindlin-1 and -2 directly bind the C-terminal region of beta integrin cytoplasmic tails and exert integrin-specific activation effects
keratinocytes derived from KS patients are unable to undergo electrotaxis, and this defect is restored by overexpression of wild-type kindlin-1 but not a W612A mutation that prevents kindlin-integrin binding.
FERMT1 activates the beta-catenin (show CTNNB1 ELISA Kits) transcriptional activity to promote EMT (show ITK ELISA Kits) in CC metastasis.
KIND1 is important not only for keratinocyte proliferation but also for the suppression of UV-induced inflammation and DNA damage.
We show a direct relationship between kindlin-1 abundance and UV-B induced apoptosis in keratinocytes, whereas kindlin-2 (show FERMT2 ELISA Kits) overexpression has no compensatory effect.
KS is caused by mutations in the FERMT1 gene. Including the present, more than 60 mutations in FERMT1 have been identified since 2003. In spite of the expanding FERMT1 mutation database, there seems to be a lack of a clear genotype-phenotype correlation in KS
A nonsense mutation in Exon 5 of KIND1 Gene in an Iranian Family may lead to incomplete and non-functional protein products and is pathogenic and has meaningful implications for the diagnosis of patients with Kindler syndrome.
we show that a certain number of KS patients may harbor FERMT1 transcriptional regulatory mutations which are not routinely detected.
Kindlin-1 is highly expressed in epithelial tissues derived from ectoderm and endoderm, whereas Kindlin-2 (show FERMT2 ELISA Kits) is mainly expressed in mesoderm-derived tissues. Likewise, Kindlin-1 was also found highly expressed in endoderm/ectoderm-derived tissues in embryos.
Kindlin1 knockdown resulted in developmental delays, gross malformations of the gut (show GUSB ELISA Kits) and eventual lethality by tadpole stages.
This gene encodes a member of the fermitin family, and contains a FERM domain and a pleckstrin homology domain. The encoded protein is involved in integrin signaling and linkage of the actin cytoskeleton to the extracellular matrix. Mutations in this gene have been linked to Kindler syndrome.
fermitin family member 1
, fermitin family homolog 1
, fermitin family homolog 1-like
, unc-112-related protein 1
, UNC112 related protein 1
, kindlin 1
, kindlin syndrome protein
, UNC-112 related protein 1