RIPK3 Antibody - #DF7339
(1)
(4)
製品説明
ソース:
Rabbit
アプリケーション:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:
*The optimal dilutions should be determined by the end user.
*Tips:
WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.
反応性:
Human,Mouse
クローナリティ:
Polyclonal
特異性:
RIPK3 Antibody detects endogenous levels of total RIPK3.
RRID:
AB_2839277
引用形式: Affinity Biosciences Cat# DF7339, RRID:AB_2839277.
引用形式: Affinity Biosciences Cat# DF7339, RRID:AB_2839277.
コンジュゲート:
Unconjugated.
精製:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
免疫原
免疫原:
A synthesized peptide derived from mouse RIPK3, corresponding to a region within the internal amino acids.
タンパク質の説明:
The product of this gene is a member of the receptor-interacting protein (RIP) family of serine/threonine protein kinases, and contains a C-terminal domain unique from other RIP family members. The encoded protein is predominantly localized to the cytoplasm, and can undergo nucleocytoplasmic shuttling dependent on novel nuclear localization and export signals. It is a component of the tumor necrosis factor (TNF) receptor-I signaling complex, and can induce apoptosis and weakly activate the NF-kappaB transcription factor.
参考文献
1). MLKL signaling regulates macrophage polarization in acute pancreatitis through CXCL10. Cell death & disease, 2023
(PubMed: 36828808)
[IF=9.0]
Application: WB Species: Mouse Sample: pancreatic acinar cells
Fig. 1 The expression of p-MLKL was upregulated in the pancreas of mice with AP and in cerulein-stimulated pancreatic acinar cells in a Ripk3-independent manner. A Immunofluorescence staining of p-MLKL (red) and p-RIPK3 (red) in the pancreas of mice (n = 3). B Immunohistochemical staining of p-MLKL in the pancreas of mice (n = 3). C Western blot of p-RIPK3, RIPK3, p-MLKL and MLKL in the pancreas of mice. GAPDH was used as the loading control (n = 6). D Immunofluorescence staining of amylase (green) colocalized with p-MLKL (red) in the pancreas of mice (n = 3). E Western blot of p-RIPK3, RIPK3, p-MLKL and MLKL in pancreatic acinar cells. GAPDH was used as the loading control (n = 7). F, G mRNA expression of Mlkl and Ripk3 in pancreatic acinar cells, data were normalized to GAPDH (n = 5–6). H Immunohistochemical staining of p-MLKL in the pancreas of WT and Ripk3-/- mice (n = 6). I Western blot of p-MLKL and MLKL in the pancreas of WT and Ripk3-/- mice. GAPDH was used as the loading control (n = 6). J Western blot of p-MLKL and MLKL in pancreatic acinar cells isolated from Ripk3-/- mice. GAPDH was used as the loading control (n = 7). K mRNA expression of Mlkl in pancreatic acinar cells isolated from Ripk3-/- mice. Data were normalized to GAPDH (n = 6). Values are shown as the means ± SEMs. ns, not significant; *P
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