Mouse TIM-3 Antibody

Detection of Mouse TIM‑3 by Western Blot. Western blot shows lysates of RAW 264.7 mouse monocyte/macrophage cell line. PVDF membrane was probed with 2 µg/mL of Goat Anti-Mouse TIM-3 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF1529) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF017). A specific band was detected for TIM-3 at approximately 45-70 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.

TIM‑3 in Mouse Spleen. TIM‑3 was detected in immersion fixed paraffin-embedded sections of mouse spleen using Goat Anti-Mouse TIM‑3 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF1529) at 3 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Goat IgG VisUCyte™ HRP Polymer Antibody (VC004). Before incubation with the primary antibody, tissue was subjected to heat-induced epitope retrieval using Antigen Retrieval Reagent-Basic (CTS013). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to lymphocytes. Staining was performed using our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents.

Detection of Mouse TIM-3 by Immunohistochemistry Blocking TIM-3 significantly reduces brain injury after hypoxia-ischaemia.(a) Representative images of TTC-stained brain slices from H/I mice treated with 100 μg of IgG (n=12) or anti-TIM-3 antibody (n=12). The infarct volume was quantified with Image J analyser and expressed as a percentage of the damaged ipsilateral hemisphere. (b) Representative magnetic resonance images (MRIs) from TIM-3-antibody-treated mice (n=4) and IgG-treated mice (n=4) at 24 h post-H/I. (c) Representative T2 images from TIM-3-antibody-treated mice (n=4) and IgG-treated mice (n=4) after H/I. (d) The extent of the oedema formation was obtained from the T2-weighted MRI images and ADC map. (e) Representative confocal microscopic images of immunohistochemical staining for NeuN and cleaved caspase-3 in coronal brain sections from IgG- and anti-TIM-3-treated H/I mice 24 h after injury. Scale bar, 50 μm. The graph shows the mean number of NeuN and cleaved caspase-3-stained cells per mm2. (f) Immunoblot detection of full-length PARP proteins in contralateral and ipsilateral cortex regions of control IgG- or anti-TIM-3-treated mice. The graph shows the relative levels of full-length PARP (116 kDa). Data represent the mean±s.d. from at least three independent experiments. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/25790768), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse TIM-3 by Immunohistochemistry Blocking TIM-3 significantly reduces brain injury after hypoxia-ischaemia.(a) Representative images of TTC-stained brain slices from H/I mice treated with 100 μg of IgG (n=12) or anti-TIM-3 antibody (n=12). The infarct volume was quantified with Image J analyser and expressed as a percentage of the damaged ipsilateral hemisphere. (b) Representative magnetic resonance images (MRIs) from TIM-3-antibody-treated mice (n=4) and IgG-treated mice (n=4) at 24 h post-H/I. (c) Representative T2 images from TIM-3-antibody-treated mice (n=4) and IgG-treated mice (n=4) after H/I. (d) The extent of the oedema formation was obtained from the T2-weighted MRI images and ADC map. (e) Representative confocal microscopic images of immunohistochemical staining for NeuN and cleaved caspase-3 in coronal brain sections from IgG- and anti-TIM-3-treated H/I mice 24 h after injury. Scale bar, 50 μm. The graph shows the mean number of NeuN and cleaved caspase-3-stained cells per mm2. (f) Immunoblot detection of full-length PARP proteins in contralateral and ipsilateral cortex regions of control IgG- or anti-TIM-3-treated mice. The graph shows the relative levels of full-length PARP (116 kDa). Data represent the mean±s.d. from at least three independent experiments. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/25790768), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse TIM-3 by Immunohistochemistry Blocking TIM-3 significantly reduces brain injury after hypoxia-ischaemia.(a) Representative images of TTC-stained brain slices from H/I mice treated with 100 μg of IgG (n=12) or anti-TIM-3 antibody (n=12). The infarct volume was quantified with Image J analyser and expressed as a percentage of the damaged ipsilateral hemisphere. (b) Representative magnetic resonance images (MRIs) from TIM-3-antibody-treated mice (n=4) and IgG-treated mice (n=4) at 24 h post-H/I. (c) Representative T2 images from TIM-3-antibody-treated mice (n=4) and IgG-treated mice (n=4) after H/I. (d) The extent of the oedema formation was obtained from the T2-weighted MRI images and ADC map. (e) Representative confocal microscopic images of immunohistochemical staining for NeuN and cleaved caspase-3 in coronal brain sections from IgG- and anti-TIM-3-treated H/I mice 24 h after injury. Scale bar, 50 μm. The graph shows the mean number of NeuN and cleaved caspase-3-stained cells per mm2. (f) Immunoblot detection of full-length PARP proteins in contralateral and ipsilateral cortex regions of control IgG- or anti-TIM-3-treated mice. The graph shows the relative levels of full-length PARP (116 kDa). Data represent the mean±s.d. from at least three independent experiments. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/25790768), licensed under a CC-BY license. Not internally tested by R&D Systems.