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The protein encoded by IL1RL1 is a member of the interleukin 1 receptor family. Additionally we are shipping IL1RL1 Proteins (24) and IL1RL1 Kits (23) and many more products for this protein.
Showing 10 out of 81 products:
Human Monoclonal IL1RL1 Primary Antibody for FACS - ABIN1107733
Burman, Jones: Treatment of HIV-related tuberculosis in the era of effective antiretroviral therapy. in American journal of respiratory and critical care medicine 2001
Show all 10 references for ABIN1107733
Human Monoclonal IL1RL1 Primary Antibody for FACS - ABIN2853578
Ikeda, Wachi, Seyama, Tajima: Effects of monensin on tropoelastin metabolism in vascular smooth muscle cells: monensin causes intracellular degradation of accumulated tropoelastin. in Journal of biochemistry 1997
Show all 10 references for ABIN2853578
Human Monoclonal IL1RL1 Primary Antibody for FACS - ABIN1107729
Tschopp, Spiegl, Didichenko, Lutmann, Julius, Virchow, Hack, Dahinden: Granzyme B, a novel mediator of allergic inflammation: its induction and release in blood basophils and human asthma. in Blood 2006
Show all 7 references for ABIN1107729
Human Polyclonal IL1RL1 Primary Antibody for EIA, IHC (p) - ABIN500811
Takeda, Kaisho, Akira: Toll-like receptors. in Annual review of immunology 2003
Show all 6 references for ABIN500811
Mouse (Murine) Polyclonal IL1RL1 Primary Antibody for WB - ABIN361230
Zhao, Ji, Wang, Gu, Song, Zhang, Liu, Chen, Zhang: Cell surface proteomics analysis indicates a neural lineage bias of rat bone marrow mesenchymal stromal cells. in BioMed research international 2014
Human Polyclonal IL1RL1 Primary Antibody for WB - ABIN2782880
Mueller, Dieplinger, Gegenhuber, Poelz, Pacher, Haltmayer: Increased plasma concentrations of soluble ST2 are predictive for 1-year mortality in patients with acute destabilized heart failure. in Clinical chemistry 2008
ST2 deletion increases inflammatory bone loss in experimental periapical lesions in mice.
ST2 receptor invalidation maintains wound inflammation, delays healing and increases fibrosis
the results of the present study suggest a possible asthma phenotype that involves the IL-33 (show IL33 Antibodies)/ST2 (show SULT2A1 Antibodies) pathway and is important for the development of airway inflammation and AHR (show AHR Antibodies) in the peripheral airways.
Data suggest that IL-33 and ST2 function as a developmental switch to license thermogenesis during the perinatal period.
The IL-33/ST2 axis may play a crucial role in the pathogenesis of angiostrongylosis.
Natural helper cells contribute to pulmonary eosinophilia by producing IL-13 via IL-33/ST2 pathway in a murine model of respiratory syncytial virus infection
Blockade of ST2 (show SULT2A1 Antibodies) markedly improves survival of lymphocytic choriomeningitis virus -infected Prf1 (show PRF1 Antibodies)-/- mice and reduces the severity of multiple disease parameters, including serum levels of IFNgamma.
the IL-33/ST2 axis specifically controls visceral adipose tissue-Treg cell development was revealed.
The activity of IL-33 at its receptor ST2 is terminated by the formation of two disulphide bridges, resulting in conformational change that disrupts the ST2 binding site.
IL-1beta (show IL1B Antibodies)-induced ST2L (show TMED1 Antibodies) expression suppressed the responsiveness of rapamycin-dendritic cells to TLR or CD40 (show CD40 Antibodies) ligation
in breast tumors from 40 female patients with absent or present tumor necrosis there was significantly higher expression of IL-33, IL-33R and VEGF in breast cancer tissues with absent tumor necrosis. Both, IL-33 and IL-33R expression correlated with VEGF expression in tumor cells.
An hyperexpression of soluble ST2 was found in Sjogren syndrome patients.
ST2 is associated with advanced and metastatic disease in GC patients and significantly correlates with the duration of the disease.
In patients with endometriosis, ST2 (show SULT2A1 Antibodies) was positively associated with VAS (show AVP Antibodies) score.
two new polymorphisms in the distal promoter region of the ST2 gene that possibly influence susceptibility to severe coronary artery disease
IL-33 and ST2 can be detected in lysates from both normal and pre-eclampsia placentas
in an unselected cohort of patients admitted to the ICU, sST2 (show SSTR2 Antibodies) was an independent predictor of 90-day all-cause mortality
The pro-T helper (Th)2 cell effects of mature IL-33 are due to differential utilization of the interleukin (IL)-33 receptor chain ST2, whereas their similar effects result from regulation of gene expression.
Expression of IL-33 receptor ST2 in human adipose tissue is increased by severe obesity indicating an autocrine action. Thus, the adipose tissue microvasculature could participate in obesity-associated inflammation and related complications via IL-33/ST2.
Elevated serum ST2 (show SULT2A1 Antibodies) (and IL-33 (show IL33 Antibodies)) were both associated with increased mortality in myocardial infarction patients.
The protein encoded by this gene is a member of the interleukin 1 receptor family. Studies of the similar gene in mouse suggested that this receptor can be induced by proinflammatory stimuli, and may be involved in the function of helper T cells. This gene, interleukin 1 receptor, type I (IL1R1), interleukin 1 receptor, type II (IL1R2) and interleukin 1 receptor-like 2 (IL1RL2) form a cytokine receptor gene cluster in a region mapped to chromosome 2q12. Alternative splicing of this gene results in multiple transcript variants.
, interleukin-1 receptor-like 1
, lymphocyte antigen 84
, protein T1
, growth stimulation-expressed
, homolog of mouse growth stimulation-expressed
, interleukin 1 receptor-related protein
, fos-responsive gene 1 protein