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mouse integrin β5 itgb5 cst 3629 cell signaling technology  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc mouse integrin β5 itgb5 cst 3629 cell signaling technology
    Mouse Integrin β5 Itgb5 Cst 3629 Cell Signaling Technology, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 99 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse integrin β5 itgb5 cst 3629 cell signaling technology/product/Cell Signaling Technology Inc
    Average 95 stars, based on 99 article reviews
    mouse integrin β5 itgb5 cst 3629 cell signaling technology - by Bioz Stars, 2026-03
    95/100 stars

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    Cell Signaling Technology Inc integrin β5
    Fig. 9. Schematic representation of the mechanism of irisin in preventing cognitive dysfunction induced by LPS or surgery. ①Exogenous irisin crosses the blood–brain barrier (BBB). ②Irisin directly targets the αVβ5 <t>integrin</t> receptor in microglia and further inhibits the expression of <t>β5</t> integrin. ③The nuclear transcription factor STAT6 is further activated to promote the polarization of microglia toward the M2 anti-inflammatory phenotype. STAT, signal transducer and activator of transcription. ④Simultaneously, STAT6 inhibits NF-κB activation, and inhibits the polarization to the M1 proinflammatory phenotype induced by LPS or surgery. NF-κB, nuclear factor kappa-B. ⑤Irisin treatment leads to increased expression of anti-inflammatory mediators (namely, IL-10 and Arg-1) and BDNF, and inhibited the expression of proinflammatory factors (namely, IL-1β, IL-18, and TNF-α), thus improving the immune microenvironment. IL, interleukin; Arg-1, arginase-1; BDNF, brain-derived neurotrophic factor. TNF, tumor necrosis factor. ⑥Irisin maintains neuronal homeostasis (including number, dendritic spine density, excitability). ⑦Irisin effectively prevents neurocognitive dysfunction in LPS-induced adult neuroinflammatory mice and surgery/anesthesia-induced early cognitive dysfunction aged mice.
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    Fig. 9. Schematic representation of the mechanism of irisin in preventing cognitive dysfunction induced by LPS or surgery. ①Exogenous irisin crosses the blood–brain barrier (BBB). ②Irisin directly targets the αVβ5 integrin receptor in microglia and further inhibits the expression of β5 integrin. ③The nuclear transcription factor STAT6 is further activated to promote the polarization of microglia toward the M2 anti-inflammatory phenotype. STAT, signal transducer and activator of transcription. ④Simultaneously, STAT6 inhibits NF-κB activation, and inhibits the polarization to the M1 proinflammatory phenotype induced by LPS or surgery. NF-κB, nuclear factor kappa-B. ⑤Irisin treatment leads to increased expression of anti-inflammatory mediators (namely, IL-10 and Arg-1) and BDNF, and inhibited the expression of proinflammatory factors (namely, IL-1β, IL-18, and TNF-α), thus improving the immune microenvironment. IL, interleukin; Arg-1, arginase-1; BDNF, brain-derived neurotrophic factor. TNF, tumor necrosis factor. ⑥Irisin maintains neuronal homeostasis (including number, dendritic spine density, excitability). ⑦Irisin effectively prevents neurocognitive dysfunction in LPS-induced adult neuroinflammatory mice and surgery/anesthesia-induced early cognitive dysfunction aged mice.

    Journal: Brain, behavior, and immunity

    Article Title: Irisin reprograms microglia through activation of STAT6 and prevents cognitive dysfunction after surgery in mice.

    doi: 10.1016/j.bbi.2024.12.019

    Figure Lengend Snippet: Fig. 9. Schematic representation of the mechanism of irisin in preventing cognitive dysfunction induced by LPS or surgery. ①Exogenous irisin crosses the blood–brain barrier (BBB). ②Irisin directly targets the αVβ5 integrin receptor in microglia and further inhibits the expression of β5 integrin. ③The nuclear transcription factor STAT6 is further activated to promote the polarization of microglia toward the M2 anti-inflammatory phenotype. STAT, signal transducer and activator of transcription. ④Simultaneously, STAT6 inhibits NF-κB activation, and inhibits the polarization to the M1 proinflammatory phenotype induced by LPS or surgery. NF-κB, nuclear factor kappa-B. ⑤Irisin treatment leads to increased expression of anti-inflammatory mediators (namely, IL-10 and Arg-1) and BDNF, and inhibited the expression of proinflammatory factors (namely, IL-1β, IL-18, and TNF-α), thus improving the immune microenvironment. IL, interleukin; Arg-1, arginase-1; BDNF, brain-derived neurotrophic factor. TNF, tumor necrosis factor. ⑥Irisin maintains neuronal homeostasis (including number, dendritic spine density, excitability). ⑦Irisin effectively prevents neurocognitive dysfunction in LPS-induced adult neuroinflammatory mice and surgery/anesthesia-induced early cognitive dysfunction aged mice.

    Article Snippet: For staining, the dHPC brain slices were washed 3 times with phosphatebuffered saline (PBS) for 5 min, blocked with a buffer containing 5 % bull serum albumin and 0.3 % Triton X-100 for 1 h, incubated with primary antibodies (1:500), including FNDC5/irisin (ab13190, Abcam), Irisin (H-067–17, Phoenix Pharmaceuticals), Iba1 (ab5076, Abcam), Integrin β5 (3629S, CST), Phospho-NF-κB p65 (3033 T, CST), NF-κB p65 (8242S, CST), STAT6 (5397; CST), Phospho-STAT6 (Tyr641) (56554; CST), c-Fos (2250 s, CST), and NeuN (ab104224, Abcam) at 4 ◦C overnight.

    Techniques: Expressing, Activation Assay, Derivative Assay