Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 11 to 13 of 13

Publication Record


TNF influences chemokine expression of macrophages in vitro and that of CD11b+ cells in vivo during Mycobacterium tuberculosis infection.
Algood HM, Lin PL, Yankura D, Jones A, Chan J, Flynn JL
(2004) J Immunol 172: 6846-57
MeSH Terms: Animals, CD11b Antigen, Cells, Cultured, Chemokine CXCL10, Chemokine CXCL9, Chemokines, Chemokines, CXC, Disease Susceptibility, Female, In Situ Hybridization, Intercellular Signaling Peptides and Proteins, Lung, Macrophages, Mice, Mice, Inbred C57BL, Tuberculosis, Tumor Necrosis Factor-alpha
Show Abstract · Added September 29, 2015
Granulomas, focal accumulations of immune cells, form in the lung during Mycobacterium tuberculosis infection. Chemokines, chemotactic cytokines, are logical candidates for inducing migration of T lymphocytes and monocytes to and within the lung. TNF influences chemokine expression in some models. TNF-deficient mice infected with M. tuberculosis are highly susceptible to disease, and granuloma formation is inhibited. Through in vitro assays, we demonstrate that neutralization of TNF in M. tuberculosis-infected macrophages led to a reduction in many inflammatory chemokines, such as C-C chemokine ligand 5, CXC ligand 9 (CXCL9), and CXCL10. In TNF-deficient mice, immune cells migrated to the lungs early after infection, but did not organize to form granulomas within the lung. Although chemokine expression, as measured in whole lung tissue, was not different, the expression of chemokines in the CD11b(+) subset of cells isolated ex vivo from the lungs of TNF-deficient mice had reduced expression of C-C chemokine ligand 5, CXCL9, and CXCL10 at early time points after TNF neutralization. Local expression of CXCR3-binding chemokines within the lungs, as determined by in situ hybridization, was also affected by TNF. Therefore, TNF affects the expression of chemokines by macrophages in vitro and CD11b(+) cells in vivo, which probably influences the local chemokine gradients and granuloma formation.
0 Communities
1 Members
0 Resources
17 MeSH Terms
Cell surface heparan sulfate participates in CXCL1-induced signaling.
Wang D, Sai J, Richmond A
(2003) Biochemistry 42: 1071-7
MeSH Terms: Animals, Binding, Competitive, CHO Cells, Cell Line, Cell Membrane, Cell Migration Inhibition, Chemokine CXCL1, Chemokine CXCL10, Chemokines, Chemokines, CXC, Chemotactic Factors, Chemotaxis, Cricetinae, Heparan Sulfate Proteoglycans, Heparitin Sulfate, Humans, Intercellular Signaling Peptides and Proteins, Protein Binding, Protein-Serine-Threonine Kinases, Receptors, Interleukin-8B, Signal Transduction, p21-Activated Kinases
Show Abstract · Added May 30, 2013
The CXC subfamily of chemokines plays an important role in diverse processes, including inflammation, wound healing, growth regulation, angiogenesis, and tumorigenesis. The ELR-CXC chemokine, CXCL1 or MGSA/GROalpha, is traditionally considered to attract neutrophils to sites of inflammation. The non-ELR-CXC chemokine, CXCL10 or IP-10, is chemotactic for monocytes, B cells, and activated T lymphocytes. In addition to its role in leukocyte migration, CXCL10 inhibits the angiogenic functions of the ELR-CXC chemokines as well as bFGF and VEGF. Heparan sulfate proteoglycans (HSPGs) are required for the interaction of bFGF and vEGF ligands and their receptors. However, the role of HSPGs in regulating the ELR-chemokines signaling and biological functions is poorly understood. We show here that the CXCL1 maximal binding to CXCR2 expressed on HEK293 and CHO-K1 cells is dependent on the presence of cell surface HSPGs. The cell surface HSPGs on cells are required for CXCL1-induced PAK1 activation. Moreover, CXCL10 can inhibit CXCL1-induced PAK1 and ERK activation as well as the CXCL1-induced chemotaxis through decreasing CXCL1 binding to cell surface heparan sulfate. These data indicate that HSPGs are involved in modulating CXCL1-induced PAK1 activation and chemotaxis through regulating CXCL1 binding activity to CXCR2 receptor. CXCL10 inhibits CXCL1-induced PAK1 activation and chemotaxis by interfering with appropriate binding of CXCL1 to CXCR2 receptor.
2 Communities
1 Members
0 Resources
22 MeSH Terms
Mob-1, a Ras target gene, is overexpressed in colorectal cancer.
Zhang R, Zhang H, Zhu W, Pardee AB, Coffey RJ, Liang P
(1997) Oncogene 14: 1607-10
MeSH Terms: Alkyl and Aryl Transferases, Cell Line, Transformed, Cell Transformation, Neoplastic, Chemokine CXCL10, Chemokines, CXC, Colorectal Neoplasms, Cytokines, Down-Regulation, Enzyme Inhibitors, Farnesyltranstransferase, Gene Expression Regulation, Neoplastic, Genes, Immediate-Early, Genes, ras, Humans, Intestinal Mucosa, Transferases
Show Abstract · Added March 27, 2014
Mutations in the ras oncogenes have been linked to many different cancers. In contrast to the extensive body of knowledge related to the genetics of ras activation, relatively little is known of the transcriptional events triggered by ras. In previous work we have used differential display to identify Mob-1, a member of alpha-chemokine family, as one of the immediate transcriptional targets following Ras activation. Here, we provide additional experimental evidence to support this finding by the use of an inducible H-ras expression system, the treatment of Ras farnesyl transferase inhibitor and activation of endogenous Ras by serum growth factors. We further demonstrate that IP-10, the human homolog of Mob-1, is overexpressed in the majority of colorectal cancers.
1 Communities
1 Members
0 Resources
16 MeSH Terms