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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Resistin like alpha

FIZZ1, found in inflammatory zone 1, HIMF, RELMalpha, hypoxia-induced mitogenic factor
may act as a hormone [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Arginase, resistin, IL-4, IL-13, TH2
Papers on FIZZ1
Protective role of G-CSF in dextran sulfate sodium-induced acute colitis through generating gut-homing macrophages.
Kim et al., London, Canada. In Cytokine, Feb 2016
In vitro, bone marrow-derived macrophages prepared in the presence of both G-CSF and macrophage colony-stimulating factor (M-CSF) (G-BMDM) expressed higher levels of regulatory macrophage markers such as programmed death ligand 2 (PDL2), CD71 and CD206, but not in arginase I, transforming growth factor (TGF)-β, Ym1 (chitinase-like 3) and FIZZ1 (found in inflammatory zone 1), and lower levels of inducible nitric oxide synthase (iNOS), CD80 and CD86 than bone marrow-derived macrophages prepared in the presence of M-CSF alone (BMDM), in response to interleukin (IL)-4/IL-13 and lipopolysaccharide (LPS)/interferon (IFN)-γ, respectively.
Hypoxia-Inducible Factor 1α Is a Critical Downstream Mediator for Hypoxia-Induced Mitogenic Factor (FIZZ1/RELMα)-Induced Pulmonary Hypertension.
Yamaji-Kegan et al., Baltimore, United States. In Arterioscler Thromb Vasc Biol, Jan 2016
We have shown that in rodents, hypoxia-induced mitogenic factor (HIMF; also known as FIZZ1 or resistin-like molecule-β) causes PH by initiating lung vascular inflammation.
IL-6 Trans-Signaling Drives Murine Crescentic GN.
Floege et al., Aachen, Germany. In J Am Soc Nephrol, Jan 2016
This correlated with increased renal mRNA synthesis of the Th17 cell cytokine IL-17A and decreased synthesis of resistin-like alpha (RELMalpha)-encoding mRNA, a surrogate marker of lesion-mitigating M2 macrophage subtypes.
The IL-33 receptor (ST2) regulates early IL-13 production in fungus-induced allergic airway inflammation.
Alber et al., Leipzig, Germany. In Mucosal Immunol, Dec 2015
In addition, alveolar macrophages upregulated the IL-33R and subsequently acquired a phenotype of alternative activation (Ym1(+), FIZZ1(+), and arginase-1(+)) linked to type 2 immunity.
NMAAP1 Expressed in BCG-Activated Macrophage Promotes M1 Macrophage Polarization.
Zhu et al., Changchun, China. In Mol Cells, Dec 2015
The current study found that the overexpression of NMAAP1 in macrophages results in M1 polarization with increased expression levels of M1 genes, such as inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-N1), Interleukin 6 (IL-6), Interleukin 12 (IL-12), Monocyte chemoattractant protein-1 (MCP-1) and Interleukin-1 beta (IL-1N2), and decreased expression of some M2 genes, such as Kruppel-like factor 4 (KLF4) and suppressor of cytokine signaling 1 (SOCS1), but not other M2 genes, including arginase-1 (Arg-1), Interleukin (IL-10), transforming growth factor beta (TGF-N2) and found in inflammatory zone 1 (Fizz1).
Temporal profile of M1 and M2 responses in the hippocampus following early 24h of neurotrauma.
Ansari, Lexington, United States. In J Neurol Sci, Nov 2015
Including shams (craniotomy only), half of the rats were assessed for gene expression and half for the protein of various markers for M1 [interferon-gamma (IFNγ), tumor necrosis factor-α (TNFα), interleukin (IL)-1-β (IL-1β), and IL-6] and M2 [IL-4, IL-10, IL-13, arginase 1 (Arg1), YM1, FIZZ1, and mannose receptor C-1 (MRC1)] responses.
FIZZ1-induced myofibroblast transdifferentiation from adipocytes and its potential role in dermal fibrosis and lipoatrophy.
Liu et al., São Paulo, Brazil. In Am J Pathol, Oct 2015
Because found in inflammatory zone 1 (FIZZ1) is an inducer of myofibroblast differentiation but an inhibitor of adipocyte differentiation, we investigated its potential role in adipocyte transdifferentiation to myofibroblast in dermal fibrosis.
Alternative activation of macrophages and pulmonary fibrosis are modulated by scavenger receptor, macrophage receptor with collagenous structure.
Carter et al., Iowa City, United States. In Faseb J, Aug 2015
Arg(432) and Arg(434) in domain V of MARCO are required for the polarization of macrophages to a profibrotic phenotype as mutation of these residues reduced FIZZ1 expression (17-fold) compared with cells expressing MARCO.
FIZZ1 Promotes Airway Remodeling in Asthma Through the PTEN Signaling Pathway.
Dong et al., Jinan, China. In Inflammation, Aug 2015
The aim of our study was to elucidate the function and signaling pathway of found in inflammatory zone 1 (FIZZ1) in airway remodeling in asthma.
TACI deficiency leads to alternatively activated macrophage phenotype and susceptibility to Leishmania infection.
Akkoyunlu et al., Silver Spring, United States. In Proc Natl Acad Sci U S A, Aug 2015
Steady-state expression levels for M2 markers IL-4Rα, CD206, CCL22, IL-10, Arg1, IL1RN, and FIZZ1 were significantly higher in TACI KO Μϕ than in WT cells.
Involvement of IGF-1 and Akt in M1/M2 activation state in bone marrow-derived macrophages.
Lynch et al., Dublin, Ireland. In Exp Cell Res, Aug 2015
In addition, differential control of the expression of mannose receptor (MRC1), arginase-1 (Arg-1), chitinase-3 like 3 (Chi3l3) and found in inflammatory zone 1 (FIZZ1) was observed.
FIZZ1 promotes airway remodeling through the PI3K/Akt signaling pathway in asthma.
Dong et al., Jinan, China. In Exp Ther Med, 2014
Found in inflammatory zone 1 (FIZZ1) plays a vital role in pulmonary inflammation and angiogenesis.
Extracellular mycobacterial DnaK polarizes macrophages to the M2-like phenotype.
Bonorino et al., Rio Grande, Brazil. In Plos One, 2013
Treatment with DnaK leads macrophages to present higher arginase I activity, IL-10 production and FIZZ1 and Ym1 expression.
Resistin-like molecule-α regulates IL-13-induced chemokine production but not allergen-induced airway responses.
Rothenberg et al., Cincinnati, United States. In Am J Respir Cell Mol Biol, 2012
identify a largely redundant functional role for Relm-alpha in acute experimental models of allergen-associated Th2 immune responses
Alternaria induces STAT6-dependent acute airway eosinophilia and epithelial FIZZ1 expression that promotes airway fibrosis and epithelial thickness.
Broide et al., San Diego, United States. In J Immunol, 2012
Alternaria induces STAT6-dependent acute airway eosinophilia and epithelial FIZZ1 expression that promotes airway fibrosis and epithelial thickness.
A therapeutic role for mesenchymal stem cells in acute lung injury independent of hypoxia-induced mitogenic factor.
Guo et al., Shanghai, China. In J Cell Mol Med, 2012
Bone marrow mesenchymal stem cells transplantation improved LPS-induced lung injury independent of hypoxia-induced mitogenic factor
[Roles of FIZZ1 and NOTCH1 in asthma].
Zhang et al., Zhengzhou, China. In Zhongguo Dang Dai Er Ke Za Zhi, 2011
FIZZl and NOTCH1 may induce an increase in a-SMA expression. FIZZl and NOTCH1 play a critical role in the process of airway remodeling.
Hypoxia-induced mitogenic factor (HIMF/FIZZ1/RELMalpha) increases lung inflammation and activates pulmonary microvascular endothelial cells via an IL-4-dependent mechanism.
Johns et al., Baltimore, United States. In J Immunol, 2010
IL-4 signaling may play a significant role in Hypoxia-induced mitogenic factor-induced lung inflammation and vascular remodeling.
Physiological significance of resistin and resistin-like molecules in the inflammatory process and insulin resistance.
Uchijima et al., Tokyo, Japan. In Curr Diabetes Rev, 2006
Resistin and RELMalpha are abundantly expressed in adipose, but RELMbeta and RELMgamma are secreted mainly from the gut.
Adiponectin and resistin--new hormones of white adipose tissue.
Bełtowski, Lublin, Poland. In Med Sci Monit, 2003
Resistin/FIZZ3 is a member of the newly discovered cysteine-reach secretory protein family, referred to as 'resistin-like molecules' (RELM) or 'found in inflammatory zone' (FIZZ), together with FIZZ1/RELMalpha and FIZZ2/RELMbeta.
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