Disease relevance of CDK5RAP3

• In this study, we analyzed the presence of antibodies directed to HIV-1 gp160, gp120, gp41, and V3 loop synthetic peptides (C51, C53, and C57 from MN and IIIB strains) utilizing the grid-blot method in PBMC cultures of 52 mother-child pairs [1].

High impact information on CDK5RAP3

• We observed a cysteine-sulfinic acid at C106 in crystalline DJ-1 but no modification of C53 or C46 [2].
• By overriding the G(2)/M checkpoint-mediated inhibition of Cdk1-cyclin B1 function, ectopic expression of C53 may represent a novel approach for chemo- and radio-sensitization of cancer cells [3].
• C53 was originally identified as a Cdk5 activator p35-binding protein and a caspase substrate [3].
• Taken together, our results strongly indicate that in response to genotoxic stress, C53 serves as an important regulatory component of the G(2)/M DNA damage checkpoint [3].
• Cdk5 activator-binding protein C53 regulates apoptosis induced by genotoxic stress via modulating the G2/M DNA damage checkpoint [3].

Biological context of CDK5RAP3

• A novel gene IC53 stimulates ECV304 cell proliferation and is upregulated in failing heart [4].
• We have identified IC53-2, a human homologue of the rat C53 gene from a human placenta cDNA library (GeneBank Accession No.AF217982) [5].
• Stable transfection of IC53 stimulates ECV304 cell proliferation by 2.1-fold compared to cells with empty vector (P<0.05) [4].
• The enzyme kinetics of the glutathione (GSH) conjugation of cryptophycin 52 (C52, R-stereoisomer) and cryptophycin 53 (C53, S-stereoisomer) by cytosolic glutathione S-transferases (cGSTs) from human, rat, mouse, dog and monkey liver were studied [6].

Anatomical context of CDK5RAP3

• The results support that IC53 is a novel gene, mainly expressed in vascular endothelial cells and mediates cell proliferation [4].
• There was little GSH conjugation of C53 by cytosol or microsomes from any species [6].

Associations of CDK5RAP3 with chemical compounds

• Substrate metabolism (especially glucose metabolism) in C53-infected cells was partially reduced by treatment with ofloxacin [7].
• C53 (delta 1-437) and C28 (delta 1-661) formed dimers irrespective of the presence or absence of 2-mercaptoethanol [8].

Other interactions of CDK5RAP3

• Among these three proteins, only C48 and C53 can be phosphorylated by Nclk, suggesting that they may be the substrates of Nclk [9].
• The full-length forms of these three novel proteins, designated C42, C48 and C53, have a molecular mass of 66, 24, and 57 kDa, respectively [9].

Analytical, diagnostic and therapeutic context of CDK5RAP3

• In an antigen-limited ELISA, only two specimens from transmitting mothers and two specimens from non-transmitting mothers had detectable 'high-affinity' antibodies to C53 at low antigen concentrations (15.4 and 8.7%, respectively; P = 0.6) [10].
• In this study, we have analysed the morphological consequences of infection of human DC by the attenuated S. typhimurium mutant strains designated PhoPc, AroA and SipB and the wild-type strains of the American Type Culture Collection (Manassas, VA, USA), ATCC 14028 and ATCC C53, by electron microscopy at 30 min, 3 h and 24 h after exposure [11].

References