FERMT2

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Fermitin family homolog 2 (FERMT2) also known as pleckstrin homology domain-containing family C member 1 (PLEKHC1) or kindlin-2 is a protein that in humans is encoded by the FERMT2 gene.[1][2][3]

Kindlin-2 is the first of the kindlin protein to be discovered in 1994. It was detected in a screen for epidermal growth factor (EGF)-induced mRNAs and initially named mitogen-inducible gene 2 (Mig-2) protein.[1]

Function

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FERMT2 is a component of extracellular matrix structures in mammalian cells and is required for proper control of cell shape change.[4]

A major task of kindlins is to regulate the activation of integrins.[5]

Interactions

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FERMT2 has been shown to interact with FBLIM1.[4]

Role in health and diseases

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  • Loss of kindlin-2 in mice leads to peri-implantation lethality.[6]
  • Kindlin-2 is highly expressed in activated myofibroblasts for regulation of focal adhesion formation.[7]
  • Deletion of Kindlin-2 retards insulin secretion and reduces β-cell mass in mice.[8]
  • Elevated kindlin-2 expression was observed in tubular intestinal fibrosis of the kidney, a condition is characterized by massive expansion of the cortical interstitium, conversion of fibroblasts into myofibroblasts and progressive EMT of tubular epithelial cells.[9]
  • Kindlin-2 is required for angiogenesis and blood vessel homeostasis.[10]
  • Kindlin-2 can exert tumor-promoting or tumor-inhibiting functions based on tumor-type-dependent.[11]
  • FERMT2 modulates the Alzheimer's Disease risk by regulating APP metabolism and Aβ peptide production.[12]


References

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  12. ^ DOI = 10.1007/s00401-016-1652-z

Further reading

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