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FN1

Developmental stage

Expressed between 12 and 19 weeks post-conception (WPC) in Bruch's membrane, with expression in the choroid evident from 14 WPC onwards (at protein level) (PubMed:29777959). Expressed in the inner limiting membrane at 17 WPC (at protein level) (PubMed:29777959). Ugl-Y1, Ugl-Y2 and Ugl-Y3 are present in the urine from 0 to 17 years of age (PubMed:17614963, PubMed:3584091).

Function

Fibronectins bind cell surfaces and various compounds including collagen, fibrin, heparin, DNA, and actin (PubMed:3024962, PubMed:3900070, PubMed:3593230, PubMed:7989369). Fibronectins are involved in cell adhesion, cell motility, opsonization, wound healing, and maintenance of cell shape (PubMed:3024962, PubMed:3900070, PubMed:3593230, PubMed:7989369). Involved in osteoblast compaction through the fibronectin fibrillogenesis cell-mediated matrix assembly process, essential for osteoblast mineralization (By similarity). Participates in the regulation of type I collagen deposition by osteoblasts (By similarity).

Anastellin

Binds fibronectin and induces fibril formation. This fibronectin polymer, named superfibronectin, exhibits enhanced adhesive properties. Both anastellin and superfibronectin inhibit tumor growth, angiogenesis and metastasis. Anastellin activates p38 MAPK and inhibits lysophospholipid signaling.

Involvement in disease

Glomerulopathy with fibronectin deposits 2

GFND2

Genetically heterogeneous autosomal dominant disorder characterized clinically by proteinuria, microscopic hematuria, and hypertension that leads to end-stage renal failure in the second to fifth decade of life.

None

The disease is caused by variants affecting the gene represented in this entry.

Spondylometaphyseal dysplasia, corner fracture type

SMDCF

An autosomal dominant form of spondylometaphyseal dysplasia, a group of short stature disorders distinguished by abnormalities in the vertebrae and the metaphyses of the tubular bones. SMDCF is characterized by flake-like, triangular, or curvilinear ossification centers at the edges of irregular metaphyses that simulate fractures. These corner fractures involve the distal tibia, the ulnar aspect of the distal radius, the proximal humerus, and the proximal femur. They represent irregular ossification at the growth plates and secondary ossification centers.

None

The disease is caused by variants affecting the gene represented in this entry.

Post-translational modifications

Sulfated.

It is not known whether both or only one of Thr-2155 and Thr-2156 are/is glycosylated.

Forms covalent cross-links mediated by a transglutaminase, such as F13A or TGM2, between a glutamine and the epsilon-amino group of a lysine residue, forming homopolymers and heteropolymers (e.g. fibrinogen-fibronectin, collagen-fibronectin heteropolymers).

Phosphorylated by FAM20C in the extracellular medium.

Proteolytic processing produces the C-terminal NC1 peptide, anastellin.

Some lysine residues are oxidized to allysine by LOXL3, promoting fibronectin activation and matrix formation.

Serotonylated on Gln residues by TGM2 in response to hypoxia.

Tissue specificity

Expressed in the inner limiting membrane and around blood vessels in the retina (at protein level) (PubMed:29777959). Plasma FN (soluble dimeric form) is secreted by hepatocytes. Cellular FN (dimeric or cross-linked multimeric forms), made by fibroblasts, epithelial and other cell types, is deposited as fibrils in the extracellular matrix. Ugl-Y1, Ugl-Y2 and Ugl-Y3 are found in urine (PubMed:17614963).

Cellular localization

  • Secreted
  • Extracellular space
  • Extracellular matrix

Alternative names

  • Fibronectin
  • FN
  • Cold-insoluble globulin
  • CIG
  • FN
  • FN1

Target type

Proteins

Primary research area

Immuno-oncology

Other research areas

  • Oncology

Molecular weight

268912Da