Coiled coil domain containing protein 120 (CCDC120), also known as JM11 protein, is a protein that, in humans, is encoded by the CCDC120gene.[1] The function of CCDC120 has not been formally identified but structural components, conservation, and interactions can be identified computationally.
The CCDC120 gene is located on human chromosome X, at Xp11.23.[2] There are six different transcript variants of CCDC120 produced by alternative splicing.[3]
Patterns
The mRNA transcript of CCDC120 contains a 120bp repeat near the 3' end.[4]
The CCDC120 protein has four different isoforms, ranging from 618 to 696 amino acids in length.[6] Isoform 1 is the longest isoform and is encoded by transcript 1 of the CCDC120 gene.[7]
Interactions
Usher Syndrome 1C Binding Protein 1, CYTH2, MDFI, Centrosomal Protein 170kDa Pseudogene 1, and Keratin 15 have all been shown experimentally to interact with CCDC120 [8] Other interactions have been identified by coexpression and datamining and can be seen in the figure.
File:CCDC120 STRING8 Interaction Network.pngShows the protein interactions for CCDC120 with experimental evidence indicated by a pink line, coexpression by dark green lines, and textmining by light green lines. This image was generated using the STRING 9.05 application. (http://string-db.org/)
The protein structure of CCDC120 is predicted to contain, as the name implies, a 65 amino acid coiled coil from positions 109-173.[10] Multiple algorithms identify 3 distinct sites where alpha-helical structures could form which are conserved in Gorilla gorilla gorilla and Danio rerio. Algorithms do not agree on any location for a beta sheet structure.[11]
Expression
Promoter
Algorithms suggest that CCDC120 has a promoter of 601bp,[12] this promoter contains a number of possible transcription factor sites as shown in the figure.
CCDC120 was found to be upregulated under pulsed electromagnetic fields in human osteoblastlike cells.[13] CCDC120 has a 7 base deletion in a Metastatic
Olfactory Neuroblastoma.[14] CCDC120 is downregulated after neonatal hypoxic-ischemic brain injury in rats.[15]
↑Kojima T, Ueda Y, Sato A, Sameshima H, Ikenoue T (February 2013). "Comprehensive gene expression analysis of cerebral cortices from mature rats after neonatal hypoxic-ischemic brain injury". J. Mol. Neurosci. 49 (2): 320–7. doi:10.1007/s12031-012-9830-5. PMID22700374.
