Disease relevance of PKIB

• Two novel full-length genes were selected for further investigation, one named human PKIbeta gene (clone 436F11, GenBank with accession number: AF225513) was over-expressed in normal brain tissues and the other named human ribosomal protein L14.22 gene (clone 507E08, GenBank with accession number: AF329277) was over-expressed in gliomas [1].

High impact information on PKIB

• Two novel members of the human cAMP-dependent protein kinase inhibitor (PKI) gene family, PKIB and PKIG, were cloned [2].
• Results also revealed that PKIbeta and calcium, which are the downstream signaling molecules, are involved in FSH regulated Sertoli cells proliferation [3].
• Regulation of FSH receptor, PKIbeta, IL-6 and calcium mobilization: Possible mediators of differential action of FSH [3].
• Assays of PKI activity demonstrated that purified PKIbeta inhibits the catalytic subunit of cAMP-dependent protein kinase [4].

Biological context of PKIB

• The PKIB and PKIG genes were mapped respectively to chromosome 6q21-22.1, using a radiation hybrid GB4 panel, and to chromosome 20q13.12-13.13, using a Stanford G3 panel [2].

Analytical, diagnostic and therapeutic context of PKIB

• FTIR, Raman spectroscopy and CD experiments implied that human PKIbeta contained only small amounts of alpha-helix and beta-structures, but large amounts of random coil and turn structures, which may explain its high thermostability [4].
• An identification method using high-performance liquid chromatography combined with electrospray mass spectrometry (HPLC-ESIMS) has been developed to verify an expressed gene product of kinase inhibitor (PKIbeta) [5].

References