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Human Polyclonal cAMP Primary Antibody for WB - ABIN1536685
Tripathi, Tecle, Verma, Crouch, White, Hartshorn: The human cathelicidin LL-37 inhibits influenza A viruses through a mechanism distinct from that of surfactant protein D or defensins. in The Journal of general virology 2012
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Chemical Monoclonal cAMP Primary Antibody for ELISA - ABIN965742
J: [SOFMER, its topicality and its prospects]. in Annales de réadaptation et de médecine physique : revue scientifique de la Société française de rééducation fonctionnelle de réadaptation et de médecine physique 2008
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these data show that LL-37 affects surface and intracellular Toll (show TLR4 Antibodies)-Like Receptor expression in tissue mast cells
This review describes novel advances involving the roles and mechanisms of human cathelicidin LL-37 in cancer.
The findings support a role for STAT3 (show STAT3 Antibodies) and HIF-1A (show HIF1A Antibodies) in the regulation of LL-37 expression.
In silico docking study have confirmed the high binding affinities of multiple 9-mer peptides derived from LL-37 to the HLA-C*06:02 molecule proposed a mechanism of the interaction between this LL-37-HLA-C*06:02 complex and T cells via TCRs.
IL-33 (show IL33 Antibodies) down-regulates the induction of hCAP-18/LL-37 production in human gingival epithelial cells.
in teens with positive recto-vaginal group B streptococcus colonization, placental mRNA expression of cathelicidin is lower compared to those who tested negative for this infection
these results suggested that human CAMP/LL-37 might act as a tumor-suppressor in OSCC and DNA methylation (show HELLS Antibodies) might play roles during carcinogenesis via directly downregulating human CAMP promoter activity.
omoted epithelial and smooth-muscle-like differentiation of Adipose-derived stem cells through activating the Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) and NF-kappaB (show NFKB1 Antibodies) pathways, respectively
Patients with type 1 diabetes and presence of microangiopathy characterize higher level of serum cathelicidin.
The expression of LL-37 was up-regulated in the inflamed mucosa of IBD patients. LL-37 was induced by TLR-3 (show TLR3 Antibodies) stimulation and exhibited an anti-microbial effect via interaction with lipopolysaccharide (LPS (show IRF6 Antibodies)).
Immunoblotting, qPCR, ChIP and siRNA-mediated gene knockdown studies revealed that the activation of phosphatidylinositol 3-kinase/protein kinase C zeta (show PRKCZ Antibodies) pathways in poly(I:C)-stimulated cells underlies Sp1 (show SP1 Antibodies) phosphorylation and recruitment to the mCRAMP promoter, leading to enhanced transcription
The effect on insulin (show INS Antibodies) resistance found in Cramp-/- mice is solely due to leukocyte infiltration and not due to inflammatory phenotype of macrophages. Therefore we conclude that cathelicidin causes insulin (show INS Antibodies) resistance by the recruitment of myeloid cells into the adipose tissue.
Cathelicidin is required for innate resistance to M. tuberculosis in a relevant animal model and is a key mediator in regulation of the levels of pro-inflammatory cytokines by calcium and cyclic nucleotides.
overexpressed CRAMP in prostate tumor initially chemoattracts early myeloid progenitors to tumor microenvironment and mediates differentiation and polarization of early myeloid progenitors into protumorigenic M2 macrophages during PCa (show ENPP1 Antibodies) progression
The aim of this project was to examine the functional impact of the human cathelicidin LL-37 and the mouse cathelicidin-related AMP (show TMPRSS5 Antibodies) (CRAMP) on the pathogenesis of lupus and arthritis.
Cathelicidin, expressed by immune cells in the tumor microenvironment, promotes colon cancer growth through activation of the PTEN/PI3K/Akt (show AKT1 Antibodies) and Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling pathways.
pancreatic beta-cells' production is controlled by short-chain fatty acids produced by the gut (show GUSB Antibodies) microbiota, and is defective in non-obese diabetic (NOD) mice
Data indicate the role of cathelicidin-related antimicrobial peptide (show CAMP Antibodies) (CRAMP) as part of the innate immune defense against pathogens in bacterial CNS infections.
Hypoxia-inducible factor-1alpha (HIF-1alpha (show HIF1A Antibodies)), a transcription factor important for activating innate immune effectors, and the antimicrobial peptide (show CAMP Antibodies) LL-37 (CRAMP in mice) are key determinants of C. albicans colonization resistance.
Specific structural motifs in syndecan-1 (show SDC1 Antibodies) HS promote Staphylococcus aureus corneal infection by inhibiting neutrophil CRAMP.
Characterization of single nucleotide polymorphisms (SNPs) and insertion-deletion (indel) polymorphisms within the bovine CATHL (show CTSL1 Antibodies) gene family.
This gene encodes a member of an antimicrobial peptide family, characterized by a highly conserved N-terminal signal peptide containing a cathelin domain and a structurally variable cationic antimicrobial peptide, which is produced by extracellular proteolysis from the C-terminus. The encoded protein has several functions in addition to antimicrobial activity, including cell chemotaxis, immune mediator induction and inflammatory response regulation.
cathelin-related antimicrobial peptide
, 18 kDa cationic antimicrobial protein
, neutrophil cationic antibacterial polypeptide of 11 kDa
, cathelin-like protein
, antibacterial peptide BMAP-34
, cathelicidin 7