Disease relevance of ABHD14B

• It was concluded that CIBP patients do have abnormal physical findings indicative of musculoskeletal disease: possibly fibrositis and/or specific myofascial syndromes, as sources of peripheral nociception [1].
• Because they did not fit the CIBP definition, patients with the following primary treatment diagnoses were eliminated: degenerative disease of the spine and spinal stenosis; degenerative disease of the hips; radiculopathy; malignancy; deafferentation pain; and miscellaneous [1].

High impact information on ABHD14B

• Insight into the mechanisms of osteoblast and osteoclast activation, via receptor activator for nuclear factor KB (RANK) dependent and independent mechanisms and a re-evaluation of primary afferent terminals within bone have led to a suggestion that CIBP may be a mixture of inflammatory and neuropathic stimuli [2].
• Coexpressed with CIBP, the antigen level of FVIII in the mammalian cell line baby hamster kidney (BHK) cells increased up to about 170% and its bioactivity rose accordingly [3].
• A gene coding for a related protein of FVIII named calcium- and integrin-binding protein (CIBP) was isolated from the normal human liver cDNA library [3].

Analytical, diagnostic and therapeutic context of ABHD14B

• Purification, crystallization and preliminary X-ray crystallographic analysis of human CCG1-interacting factor B [4].
• These findings question the validity of the CIBP concept and point to the need for a careful, all-inclusive physical examination as a basic initial requirement in the classification of chronic pain patients [1].
• The gene coding for CIBP was constructed by polymerase chain reaction (PCR) and then cotransfected with the B-domain-deleted FVIII gene into mammalian cell lines using the expression vector of FVIII for transient or stable expression [3].

References