As a positive regulator of collagen fibrillogenesis, it is probably involved in the organization and remodeling of the extracellular matrix. May positively regulate MAP-kinase activity in adipocytes, leading to enhanced adipocyte proliferation and reduced adipocyte differentiation. May also positively regulate NF-kappa-B activity in macrophages by promoting the phosphorylation and subsequent degradation of I-kappa-B-alpha (NFKBIA), leading to enhanced macrophage inflammatory responsiveness. Can act as a transcriptional repressor. Isoform 1: Interacts with different types of collagen, including collagens I, III, and V (By similarity). Isoform 2: Interacts with GNG5, NFKBIA, MAPK1, MAPK3 and PTEN. Interaction with MAPK1 may stimulate DNA-binding. May interact with calmodulin. Binds to DNA in vitro. Isoform 1 and isoform 2 are expressed in adipose tissue, brain, heart, kidney, liver, lung, skeletal muscle, small intestine, spleen and testis. Isoform 2 is expressed in macrophages. Expressed in aorta, preadipocytes, adipocyte tissue, brain, heart, liver, lung, skeletal muscle, skin and spleen (at protein level). Expressed in the somites and dorsa from 9.5 dpc and in the yolk sac and embryonic vasculature from 10.5 dpc. Expression within the large and small blood vessels increases at 11.5 dpc and 13.5 dpc, with high expression in the vascular smooth muscle at 16.5 dpc. Also expressed later in development in mesenchymal cells in the dermal layer, the developing skeleton, connective tissue and the umbilical ring and vessels. Up-regulated during vascular smooth muscle cell differentiation and down-regulated during adipocyte differentiation and osteoblast differentiation. By TGF-beta. Expression is also induced by a high fat diet. The F5/8 type C domain binds to different types of collagen, including collagens I, III, and V. Phosphorylated by MAPK1 in vitro. Two independent knockout mice have been generated for the gene encoding this protein, and these exhibit different phenotypes. Mice lacking exons 7-12 exhibit reduced growth rate and body weight and resistance to dietary-induced obesity. Individual adipocytes from these animals are hypoproliferative while the adipose tissue is prone to apoptosis. Mice lacking exons 7-16 die perinatally from gastroschisis, in which abdominal viscera are extruded through the ventral body wall. Surviving mice exhibit deficient wound healing, having dermal fibroblasts with reduced proliferative capacity. Mice lacking exons 7-16 may exhibit phenotypes arising from effects on the locus encoding Pold2, which lies immediately downstream of this locus. Belongs to the peptidase M14 family. Although related to peptidase M14 family, lacks the active site residues and zinc-binding sites, suggesting that it has no carboxypeptidase activity.