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anti timp1  (R&D Systems)


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    R&D Systems anti timp1
    Anti Timp1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 56 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+timp1/pm40209863-130-25-26?v=R%26D+Systems
    Average 94 stars, based on 56 article reviews
    anti timp1 - by Bioz Stars, 2026-07
    94/100 stars

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    Fig. 11. Schematic diagram of EZH2-mediated <t>TIMP1</t> suppression in GABAergic interneurons driving spinal microglia activation through MMP-9-TLR2/4-NLRP3 signaling in neuropathic pain. TIMP1 deficiency in spinal GABAergic interneurons contributes to the activation of MMP-9 in the spinal cord, which, in turn, acti vates microglia and induces IL-1β maturation via an TLR2/4-NLRP3 dependent pathway. The suppression of Timp1 is linked to epigenetic silencing mechanisms in neuropathic pain. Substance P, released from primary sensory neurons, triggers the transcriptional suppression of Timp1 in spinal GABAergic interneurons by upregulating EZH2 expression and increasing H3K27me3 enrichment at the Timp1 promoter.
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    Fig. 11. Schematic diagram of EZH2-mediated <t>TIMP1</t> suppression in GABAergic interneurons driving spinal microglia activation through MMP-9-TLR2/4-NLRP3 signaling in neuropathic pain. TIMP1 deficiency in spinal GABAergic interneurons contributes to the activation of MMP-9 in the spinal cord, which, in turn, acti vates microglia and induces IL-1β maturation via an TLR2/4-NLRP3 dependent pathway. The suppression of Timp1 is linked to epigenetic silencing mechanisms in neuropathic pain. Substance P, released from primary sensory neurons, triggers the transcriptional suppression of Timp1 in spinal GABAergic interneurons by upregulating EZH2 expression and increasing H3K27me3 enrichment at the Timp1 promoter.
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    Fig. 11. Schematic diagram of EZH2-mediated <t>TIMP1</t> suppression in GABAergic interneurons driving spinal microglia activation through MMP-9-TLR2/4-NLRP3 signaling in neuropathic pain. TIMP1 deficiency in spinal GABAergic interneurons contributes to the activation of MMP-9 in the spinal cord, which, in turn, acti vates microglia and induces IL-1β maturation via an TLR2/4-NLRP3 dependent pathway. The suppression of Timp1 is linked to epigenetic silencing mechanisms in neuropathic pain. Substance P, released from primary sensory neurons, triggers the transcriptional suppression of Timp1 in spinal GABAergic interneurons by upregulating EZH2 expression and increasing H3K27me3 enrichment at the Timp1 promoter.
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    Fig. 11. Schematic diagram of EZH2-mediated TIMP1 suppression in GABAergic interneurons driving spinal microglia activation through MMP-9-TLR2/4-NLRP3 signaling in neuropathic pain. TIMP1 deficiency in spinal GABAergic interneurons contributes to the activation of MMP-9 in the spinal cord, which, in turn, acti vates microglia and induces IL-1β maturation via an TLR2/4-NLRP3 dependent pathway. The suppression of Timp1 is linked to epigenetic silencing mechanisms in neuropathic pain. Substance P, released from primary sensory neurons, triggers the transcriptional suppression of Timp1 in spinal GABAergic interneurons by upregulating EZH2 expression and increasing H3K27me3 enrichment at the Timp1 promoter.

    Journal: Brain, behavior, and immunity

    Article Title: EZH2-mediated suppression of TIMP1 in spinal GABAergic interneurons drives microglial activation via MMP-9-TLR2/4-NLRP3 signaling in neuropathic pain.

    doi: 10.1016/j.bbi.2025.04.007

    Figure Lengend Snippet: Fig. 11. Schematic diagram of EZH2-mediated TIMP1 suppression in GABAergic interneurons driving spinal microglia activation through MMP-9-TLR2/4-NLRP3 signaling in neuropathic pain. TIMP1 deficiency in spinal GABAergic interneurons contributes to the activation of MMP-9 in the spinal cord, which, in turn, acti vates microglia and induces IL-1β maturation via an TLR2/4-NLRP3 dependent pathway. The suppression of Timp1 is linked to epigenetic silencing mechanisms in neuropathic pain. Substance P, released from primary sensory neurons, triggers the transcriptional suppression of Timp1 in spinal GABAergic interneurons by upregulating EZH2 expression and increasing H3K27me3 enrichment at the Timp1 promoter.

    Article Snippet: The primary antibodies were specific for β-actin (ABclonal, AC026, 1:10000, Wuhan, China), Histone H3 (ABclonal, A2348, 1:1000, Wuhan, China), TriMethyl-Histone H3-K27 (H3K27me3) (ABclonal, A2363, 1:1000, Wuhan, China), EZH2 (ABclonal, A16846, 1:1000, Wuhan, China), tissue inhibitor of metalloproteinase 1 (TIMP1) (R&D Systems, AF980, 0.1 μg/mL), TIMP1 (immunoway, YT4658, 1:500), MMP-9 (ABclonal, A0289, 1:1000, Wuhan, China), IL1β (ABmart, P50520-1R1, 1:800, Shanghai, China), NLRP3 (Adipogen, AG-20B0014-C100, 1:500), caspase-1 (p20; Adipogen, AG-20B-0042-C100, 1:500), NF-κB p65 (ABclonal, A2547, 1:1000, Wuhan, China), phospho-NF-κB p65 (ABclonal, AP0124, 1:1000, Wuhan, China), TLR2 (proteintech, 66645–1-Ig, 1:500) and TLR4 (proteintech, 66350–1-Ig, 1:1000).

    Techniques: Activation Assay, Expressing