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
[edit | edit source]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
[edit | edit source]FERMT2 has been shown to interact with FBLIM1.[4]
Role in health and diseases
[edit | edit source]- 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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Further reading
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External links
[edit | edit source]- FERMT2 Info with links in the Cell Migration Gateway Archived 2014-12-11 at the Wayback Machine
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