Disease relevance of Grcc10

• Two serine/threonine protein kinases were compared in C10, a clone from the nontumorigenic NAL IA cell line derived from normal mouse lung epithelium, and PCC4, a cell line derived from a mouse lung adenoma [1].
• In two patients with neutrophil-specific granule deficiency, less than 1% of the neutrophils were found to be C10 positive, while neutrophils from a patient with idiopathic leukemoid reaction and recurrent infections demonstrated greater than 99% C10 binding [2].
• Wool fatty alcohols (WF-Alc; C10-C33), separated by esterolysis of wool grease secreted from sheep sebaceous gland, inhibited growth of mouse Ehrlich ascites carcinoma (EAC) cells in contrast to no inhibition by unesterolysed wool grease [3].

High impact information on Grcc10

• Cytosolic protein kinase C (PKC) specific activity was lower in PCC4 cells than in C10 cells, but particulate PKC activity was similar in the two cell lines [1].
• In contrast, TPA caused a generalized increase in the phosphorylation of most membrane proteins in C10 cells [1].
• In addition, PCC4 cells had less mRNA coding for the R1 regulatory subunit of cyclic AMP (cAMP)-dependent protein kinase (PKA) than C10 cells, as determined by Northern blotting using an R1 alpha cDNA probe [1].
• Both measurements of PKC activity and immunoblotting assays using anti-PKC antisera showed increased particulate PKC in TPA-treated C10 cells resulting from a quantitative translocation of PKC molecules from cytoplasm to plasma membrane [1].
• The expression of the C10 message in response to cytokines was completely blocked by cycloheximide, whereas the other three chemokines were all overexpressed in the presence of this inhibitor [4].

Biological context of Grcc10

• Cluster C, which probably contains the binding site for the CD30 ligand, was defined by Ki-3, M44, HeFi-I and C10 [5].
• Studies of NBT reduction, phagocytosis, adherence, light scattering characteristics, and monoclonal antibody surface binding have failed to demonstrate physical or functional differences between the C10-defined populations [2].
• In contrast to results using unexposed C10 cells or cells exposed to the nonpathogenic particle glass beads, flow cytometry showed increased numbers of hypodiploid cells and cells in S phase after addition of DQ12 quartz or CMDs [6].
• In contrast to that seen in tumor cells, alkylation at both N10 and C10 reduced influx potential (increased Km) in isolated intestinal epithelial cells from mouse small intestine [7].
• The gene for C10, a member of the beta-chemokine family of cytokines, contains a novel second exon encoding a 16 amino acid sequence which is inserted into the amino-terminal region of the protein [8].

Anatomical context of Grcc10

• We examined the expression in primary macrophages of a recently described, and as yet functionally uncharacterized, murine beta chemokine, C10, and contrasted its regulation with that of several other beta chemokines [4].
• Ia expression by keratinocytes was associated with the increased epidermal invasion of BB5 cells, but did not render C10 cells capable of migrating into the epidermis [9].
• We have investigated this pathway in paired transformed/nontransformed cell lines from murine peripheral lung epithelium, E9/E10 and A5/C10 [10].
• The role of Ia+ keratinocytes in epidermotropism of T cells was analyzed by using self-IA specific autoreactive cloned T cells with epidermotropic nature (termed BB5) and those without it (termed C10) [9].
• We have modeled this effect by examining the interactions of 7r,8t-dihydroxy-9t,10t-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE) with sulfite, the physiological form of SO2, in a murine respiratory epithelial cell line (C10) [11].

Associations of Grcc10 with chemical compounds

• Inhibition was detected in WB-F344 cells at BHT concentrations > or = 62.5 microM and in C10 cells at concentrations > or = 150 microM after 4 h treatment [12].
• These results suggest that oxidation at position C10 is at least partially responsible for the inhibition of EGF binding induced by chrysarobin [13].
• The ability of C10-substituted derivatives of anthralin to undergo base catalyzed oxidation in vitro correlated with both ODC inducing and tumor promoting activities [14].
• We exposed C10 cells to [3H]-anti-BPDE and determined the effects of 1 and 10 mM sulfite on the uptake and subcellular localization of labeled products [11].
• Three mammary tumor lines, all derived in our laboratory from a spontaneous C3H mammary tumor were employed: T-58 (uncloned parental line, having weak lung metastasizing ability from the subcutaneous site), C3 (a clone of T-58, showing high metastatic ability), and C10 (a nonmetastatic clone of T-58) [15].

Analytical, diagnostic and therapeutic context of Grcc10

• Ki-2 to Ki-7 and the other anti-CD30 antibodies Ki-I, Ber-H2, HeFi-I, M44, M67, HRS-I, HRS-4 and C10 were employed for epitope mapping [5].
• Antibody C10 produced conjugate which rendered the Elisa as sensitive as a commercially obtainable immunoradiometric assay with which it was compared [16].
• Control groups were added at 10 (C10) and 32 weeks (C32), as well as a group that received only methimazole (CM10) [17].

References