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The protein encoded by FIL1d is a member of the interleukin 1 cytokine family. Zusätzlich bieten wir Ihnen Interleukin 1 delta Kits (28) und Interleukin 1 delta Proteine (27) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal FIL1d Primary Antibody für IHC, IHC (p) - ABIN4325558
Frey, Derer, Messbacher, Baeten, Bugatti, Montecucco, Schett, Hueber: The novel cytokine interleukin-36α is expressed in psoriatic and rheumatoid arthritis synovium. in Annals of the rheumatic diseases 2013
Interleukin-36 (zeige IL1F6 Antikörper) (IL-36) ligands require processing for full agonist (IL-36alpha, IL-36beta, and IL-36gamma) or antagonist (IL-36Ra) activity
Transcripts for IL-1F5 are significantly increased in the involved skin of bi- and monotransgenic mice compared with their C57BL controls.
IL-1F5 has unique loop conformations for receptor binding specificity
IL-1F5 mediates anti-inflammatory effects through its ability to induce interleukin-4 (zeige IL4 Antikörper) production, as a consequence of its interaction with orphan receptor (zeige NR1D2 Antikörper) single Ig IL-1R-related molecule (SIGIRR)/TIR8 (zeige SIGIRR Antikörper).
IL36RN may be the major disease-causing gene in generalized pustular psoriasis patients in Han population in Sichuan region of China.
IL36RN mutations were strongly linked with early onset and hyponychial pustules, but not with therapeutic efficacy of acitretin or recurrence frequency. Early onset and hyponychial pustules may be specific to IL36RN mutation, however this alone is an insufficient biomarker for acitretin therapy.
Using different blood leukocyte and skin resident cell preparations, and recombinant proteins, the authors have identified that neutrophil elastase (zeige ELANE Antikörper), but not other neutrophil derived proteases, cleaves IL-36Ra into its highly active antagonistic form.
A study on the association of IL36RN mutations that affect protein expression and function with phenotype in patients with generalized pustular psoriasis.
The findings indicate that IL36RN mutations do not seem to contribute to the pathogenesis of common, nonpustular forms of psoriasis, but to the rarer pustular manifestations such as GPP, acrodermatitis continua suppurativa of Hallopeau and acute generalized exanthematous pustulosis.
Some cases of geographic tongue are caused by IL36RN mutations, while those lacking mutations are associated with an imbalance in expression between IL-36Ra and IL-36gamma proteins in tongue tissue.
Study data and the previous European study suggest that palmoplantar pustulosis is not associated with mutations of the IL36RN gene.
Case Report: short-term infliximab for treatment of juvenile generalized pustular psoriasis with IL36RN mutation.
The authors present a case of strikingly distinct phenotypes seen in two IL36RN mutation carriers from the same nonconsanguineous pedigree. This mutation it appears may influence the age of onset.
We identified a novel homozygous missense mutation in IL36RN in two siblings, and showed the molecular basis of the condition to be both distinct from psoriasis and distinct between the two families studied.
Is a highly and a specific antagonist of the IL-1 receptor-related protein 2-mediated response to interleukin 1 family member 9 (IL1F9). Could constitute part of an independent signaling system analogous to interleukin-1 alpha (IL-1A), beta (IL-1B) receptor agonist and interleukin-1 receptor type I (IL- 1R1), that is present in epithelial barriers and takes part in local inflammatory response.
, interleukin 1 receptor antagonist homolog 1
, interleukin-1 HY1
, interleukin-1 delta
, interleukin-1 family member 5
, interleukin-1 homolog 3
, interleukin-1-like protein 1
, interleukin-36 receptor antagonist protein
, IL-1 related protein 3
, IL-1F5 (IL-1HY1, FIL1-delta, IL-1RP3, IL-1L1, IL-1-delta)
, IL-1ra homolog 1
, IL1F5 (Canonical product IL-1F5a)
, interleukin 1 family, member 5 (delta)
, interleukin-1 receptor antagonist homolog 1