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           Search results for: Recombinant Human GRO-alpha CXCL1 Proteins    

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Plasma levels of growth-related oncogene (CXCL1-3) associated with fibrosis and platelet counts in HCV-infected patients.

Fibrosis progression in hepatitis C virus (HCV)-infected patients varies greatly between individuals. Chemokines recruit immune cells to the infected liver and may thus play a role in the fibrosis process.

1232 related Products with: Plasma levels of growth-related oncogene (CXCL1-3) associated with fibrosis and platelet counts in HCV-infected patients.

Prolactin-Inducible Prote Bovine Androstenedione,AS Mouse Insulin-like Growth Apoptosis Phospho-Specifi Rabbit Plasma US Origin I Rabbit Plasma US Origin I Rabbit Plasma US Origin I Rat monoclonal anti mouse Interleukins Recombinant Human Platelet Derived Gr Tyrosine Kinase Adaptors Rabbit Plasma US Origin I

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Epigenetics underpinning the regulation of the CXC (ELR+) chemokines in non-small cell lung cancer.

Angiogenesis may play a role in the pathogenesis of Non-Small Cell Lung cancer (NSCLC). The CXC (ELR(+)) chemokine family are powerful promoters of the angiogenic response.

2975 related Products with: Epigenetics underpinning the regulation of the CXC (ELR+) chemokines in non-small cell lung cancer.

Lung non small cell cance Non-small cell lung cance Non small cell lung carci Non small cell lung carci Multiple lung carcinoma ( High density non small ce Lung small cell carcinoma Small cell lung carcinoma Middle advanced stage lun Non small cell lung carci Lung cancer and adjacent GLP 2 ELISA Kit, Rat Prog

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A chemokine-degrading extracellular protease made by group A Streptococcus alters pathogenesis by enhancing evasion of the innate immune response.

Circumvention of the host innate immune response is critical for bacterial pathogens to infect and cause disease. Here we demonstrate that the group A Streptococcus (GAS; Streptococcus pyogenes) protease SpyCEP (S. pyogenes cell envelope protease) cleaves granulocyte chemotactic protein 2 (GCP-2) and growth-related oncogene alpha (GROalpha), two potent chemokines made abundantly in human tonsils. Cleavage of GCP-2 and GROalpha by SpyCEP abrogated their abilities to prime neutrophils for activation, detrimentally altering the innate immune response. SpyCEP expression is negatively regulated by the signal transduction system CovR/S. Purified recombinant CovR bound the spyCEP gene promoter region in vitro, indicating direct regulation. Immunoreactive SpyCEP protein was present in the culture supernatants of covR/S mutant GAS strains but not in supernatants from wild-type strains. However, wild-type GAS strains do express SpyCEP, where it is localized to the cell wall. Strain MGAS2221, an organism representative of the highly virulent and globally disseminated M1T1 GAS clone, differed significantly from its isogenic spyCEP mutant derivative strain in a mouse soft tissue infection model. Interestingly, and in contrast to previous studies, the isogenic mutant strain generated lesions of larger size than those formed following infection with the parent strain. The data indicate that SpyCEP contributes to GAS virulence in a strain- and disease-dependent manner.

1603 related Products with: A chemokine-degrading extracellular protease made by group A Streptococcus alters pathogenesis by enhancing evasion of the innate immune response.

Mouse Anti-Streptococcus Rabbit Anti-Streptococcus Goat Anti-Streptococcus G Rabbit Anti-Streptococcus Mouse Anti-Streptococcus Rabbit Anti-Streptococcus Goat Anti-Streptococcus G Rabbit Anti-Streptococcus Mouse Anti-Streptococcus Rabbit Anti-Streptococcus CAR,CAR,Constitutive acti Goat Anti-Streptococcus G

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Coordinate upregulation of interleukin-8 and growth-related gene product-alpha is present in the colonic mucosa of inflammatory bowel.

Although ãlpha-chemokines, such as interleukin (IL)-8 and epithelial neutrophil-activating peptide 78, are implicated in the pathogenesis of inflammatory bowel disease (IBD), little information is currently available on the expression and cellular source of growth-related gene product-alpha (GROalpha) and its functional relationship to other ãlpha-chemokines in the intestinal mucosa of patients with IBD.

1030 related Products with: Coordinate upregulation of interleukin-8 and growth-related gene product-alpha is present in the colonic mucosa of inflammatory bowel.

Goat Anti- TRIM5 RNF88 (a Rabbit Anti-Integrin alph Rabbit Anti-Integrin alph Interleukin-34 IL34 (N-t Rabbit Anti-G protein alp Rabbit Anti-Integrin alph Rabbit Anti-G protein alp Rabbit Anti-CD11b Integri Mouse Anti-Human Interleu Sheep interleukin 2 recep Rabbit Anti-Insulin Recep ELISA Human , Interleukin

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IL-17 stimulates intraperitoneal neutrophil infiltration through the release of GRO alpha chemokine from mesothelial cells.

IL-17 is a newly discovered cytokine implicated in the regulation of hemopoiesis and inflammation. Because IL-17 production is restricted to activated T lymphocytes, the effects exerted by IL-17 may help one to understand the contribution of T cells to the inflammatory response. We investigated the role of IL-17 in leukocyte recruitment into the peritoneal cavity. Leukocyte infiltration in vivo was assessed in BALB/Cj mice. Effects of IL-17 on chemokine generation in vitro were examined in human peritoneal mesothelial cells (HPMC). Administration of IL-17 i.p. resulted in a selective recruitment of neutrophils into the peritoneum and increased levels of KC chemokine (murine homologue of human growth-related oncogene alpha (GROalpha). Pretreatment with anti-KC Ab significantly reduced the IL-17-driven neutrophil accumulation. Primary cultures of HPMC expressed IL-17 receptor mRNA. Exposure of HPMC to IL-17 led to a dose- and time-dependent induction of GROalpha mRNA and protein. Combination of IL-17 together with TNF-alpha resulted in an increased stability of GROalpha mRNA and synergistic release of GROalpha protein. Anti-IL-17 Ab blocked the effects of IL-17 in vitro and in vivo. IL-17 is capable of selectively recruiting neutrophils into the peritoneal cavity via the release of neutrophil-specific chemokines from the peritoneal mesothelium.

1463 related Products with: IL-17 stimulates intraperitoneal neutrophil infiltration through the release of GRO alpha chemokine from mesothelial cells.

RABBIT ANTI HUMAN SDF-1 A Epidermal Growth Factor ( alpha DGal(1 4) DGal CETE N alpha 4 Tosyl L arginin Epidermal Growth Factor ( (S) ( ) N Benzyl alpha me alpha-Bromo-p-tolunitrile Recombinant Human PKC alp Rabbit Anti-Integrin alph Human MIP-3 alpha ELISA E 3 Methoxyphenylacetic aci C-C Chemokine Receptor 3

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MGSA/GRO-mediated melanocyte transformation involves induction of Ras expression.

The MGSA/GRO protein is endogenously expressed in almost 70% of the melanoma cell lines and tumors, but not in normal melanocytes. We have previously demonstrated that over-expression of human MGSA/GROalpha, beta or gamma in immortalized murine melanocytes (melan-a cells) enables these cells to form tumors in SCID and nude mice. To examine the possibility that the MGSA/GRO effect on melanocyte transformation requires expression of other genes, differential display was performed. One of the mRNA's identified in the screen as overexpressed in MGSA/GRO transformed melan-a clones was the newly described M-Ras or R-Ras3 gene, a member of the Ras gene superfamily. Over-expression of MGSA/GRO upregulates M-Ras expression at both the mRNA and protein levels, and this induction requires an intact glutamine-leucine-arginine (ELR)-motif in the MGSA/GRO protein. Western blot examination of Ras expression revealed that K- and N-Ras proteins are also elevated in MGSA/GRO-expressing melan-a clones, leading to an overall increase in the amount of activated Ras. MGSA/GRO-expressing melan-a clones exhibited enhanced AP-1 activity. The effects of MGSA/GRO on AP-1 activation could be mimicked by over-expression of wild-type M-Ras or a constitutively activated M-Ras mutant in control melan-a cells as monitored by an AP-1-luciferase reporter, while expression of a dominant negative M-Ras blocked AP-1-luciferase activity in MGSA/GRO-transformed melan-a clones. In the in vitro transformation assay, over-expression of M-Ras mimicked the effects of MGSA/GRO by inducing cellular transformation in control melan-a cells, while over-expression of dominant negative M-Ras in MGSA/GROalpha-expressing melan-a-6 cells blocked transformation. These data suggest that MGSA/GRO-mediated transformation requires Ras activation in melanocytes.

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pCAMBIA1305.1 Vector (Gus pCAMBIA1391 Vector (gusA Rasagiline mesylate CAS: Expression Media Products RASGRP4 & RAP1A Protein P removed without changing Goat Anti-Human RASSF7 HR Mouse Anti-Human Melanocy pSV40beta Mammalian lacZc pDC99 Mammalian Luciferas pCAMBIA1200 Vector (No Re pCAMBIA1302 Vector (mgfp5

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