C1q/TNF-Related Protein 3 (CTRP3) Function and Regulation

Abstract

As the largest endocrine organ, adipose tissue secretes many bioactive molecules that circulate in blood, collectively termed adipokines. Efforts to identify such metabolic regulators have led to the discovery of a family of secreted proteins, designated as C1q tumor necrosis factor (TNF)-related proteins (CTRPs). The CTRP proteins, adiponectin, TNF-alpha, as well as other proteins with the distinct C1q domain are collectively grouped together as the C1q/TNF superfamily. Reflecting profound biological potency, the initial characterization of these adipose tissue-derived CTRP factors finds wide-ranging effects upon metabolism, inflammation, and survival-signaling in multiple tissue types. CTRP3 (also known as CORS26, cartducin, or cartonectin) is a unique member of this adipokine family. In this review we provide a comprehensive overview of the research concerning the expression, regulation, and physiological function of CTRP3. © 2017 American Physiological Society. Compr Physiol 7:863-878, 2017.

Figure 1

Structural overview of CTRP3. (A) Two splice variants were identified and designated as CTRP3A and CTRP3B. (B) Organization of the CTRP3A and CTRP3B genes and proteins. The human CTRP3A gene is 25.3 kb in size, consists of six exons and five introns, and is located on chromosome 5p13. Exons 1, 2, 3, 4, 5, and 6 of the CTRP3A gene are 171, 112, 155, 130, 100, and 2885 bp in size, respectively. The size of each intron is also indicated. Exon 1B (gray square) contains a 219-nucleotide sequence found in CTRP3B cDNA, coding for an extra 73 amino acid residues. A potential Nlinked glycosylation site is circled. The consensus splice donors are shown in italic type. This figure was originally published in The Journal of Biological Chemistry (51) and image reproduced according to the copyright policy of the ASBMB. © the American Society for Biochemistry and Molecular Biology.