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Is a highly and a specific antagonist of the IL-1 receptor-related protein 2-mediated response to interleukin 1 family member 9 (IL1F9). 再加上，我们可以发Interleukin 1 delta 抗体 (76) 和 Interleukin 1 delta 试剂盒 (25)和数多这个蛋白质的别的产品。
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Interleukin-36 (显示 IL1F6 蛋白) (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 (显示 IL4 蛋白) production, as a consequence of its interaction with orphan receptor (显示 NR1D2 蛋白) single Ig IL-1R-related molecule (SIGIRR)/TIR8 (显示 SIGIRR 蛋白).
Using different blood leukocyte and skin resident cell preparations, and recombinant proteins, the authors have identified that neutrophil elastase (显示 ELANE 蛋白), 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.
generalized pustular psoriasis and early onset, ever generalized pustular psoriasis (more than two attacks), ever acrodermatitis continua of Hallopeau, inverse psoriasis, and a family history of pustular psoriasis were associated with IL36RN mutation.
IL36RN was identified as strong regulators of skin pathology in both lesional and non-lesional skin samples.
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