MLKL Antibody - #DF7412

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产品: MLKL 抗体
货号: DF7412
描述: Rabbit polyclonal antibody to MLKL
应用: WB IHC IF/ICC
反应: Human, Mouse, Rat
分子量: 54kDa; 54kD(Calculated).
蛋白号: Q8NB16
RRID: AB_2839350

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 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

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IF/ICC Protocol

产品描述

来源:
Rabbit
应用:
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:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human,Mouse,Rat
克隆:
Polyclonal
特异性:
MLKL Antibody detects endogenous levels of total MLKL.
RRID:
AB_2839350
引用格式: Affinity Biosciences Cat# DF7412, RRID:AB_2839350.
偶联:
Unconjugated.
纯化:
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.
别名:

展开/折叠

9130019I15Rik; FLJ34389; hMLKL; Mixed lineage kinase domain like; Mixed lineage kinase domain like protein; Mixed lineage kinase domain like pseudokinase; Mixed lineage kinase domain-like protein; Mlkl; MLKL_HUMAN;

抗原和靶标

免疫原:
Uniprot:

Q8NB16(MLKL_HUMAN) >>Visit HPA database.

基因/基因ID:
MLKL(197259)
序列:
MENLKHIITLGQVIHKRCEEMKYCKKQCRRLGHRVLGLIKPLEMLQDQGKRSVPSEKLTTAMNRFKAALEEANGEIEKFSNRSNICRFLTASQDKILFKDVNRKLSDVWKELSLLLQVEQRMPVSPISQGASWAQEDQQDADEDRRAFQMLRRDNEKIEASLRRLEINMKEIKETLRQYLPPKCMQEIPQEQIKEIKKEQLSGSPWILLRENEVSTLYKGEYHRAPVAIKVFKKLQAGSIAIVRQTFNKEIKTMKKFESPNILRIFGICIDETVTPPQFSIVMEYCELGTLRELLDREKDLTLGKRMVLVLGAARGLYRLHHSEAPELHGKIRSSNFLVTQGYQVKLAGFELRKTQTSMSLGTTREKTDRVKSTAYLSPQELEDVFYQYDVKSEIYSFGIVLWEIATGDIPFQGCNSEKIRKLVAVKRQQEPLGEDCPSELREIIDECRAHDPSVRPSVDEILKKLSTFSK

翻译修饰 - Q8NB16 作为底物

Site PTM Type Enzyme
K40 Ubiquitination
K50 Ubiquitination
S52 Phosphorylation
K57 Ubiquitination
T59 Phosphorylation
K66 Ubiquitination
K78 Ubiquitination
S92 Phosphorylation
S106 Phosphorylation
S125 Phosphorylation
S128 Phosphorylation
K157 Ubiquitination
S161 Phosphorylation
K173 Ubiquitination
K183 Ubiquitination
K198 Ubiquitination
K219 Ubiquitination
K230 Ubiquitination
T246 Phosphorylation
K249 Ubiquitination
T302 Phosphorylation
K331 Ubiquitination
S334 Phosphorylation
K354 Acetylation
K354 Ubiquitination
T357 Phosphorylation Q9Y572 (RIPK3)
S358 Phosphorylation Q9Y572 (RIPK3)
T364 Phosphorylation
K372 Ubiquitination
S373 Phosphorylation
T374 Phosphorylation
S393 Phosphorylation
S417 Phosphorylation
S467 Phosphorylation

研究背景

功能:

Pseudokinase that plays a key role in TNF-induced necroptosis, a programmed cell death process. Activated following phosphorylation by RIPK3, leading to homotrimerization, localization to the plasma membrane and execution of programmed necrosis characterized by calcium influx and plasma membrane damage. Does not have protein kinase activity. Binds to highly phosphorylated inositol phosphates such as inositolhexakisphosphate (InsP6) which is essential for its necroptotic function.

翻译修饰:

Phosphorylation by RIPK3 induces a conformational switch that is required for necroptosis. It also induces homotrimerization and localization to the plasma membrane.

细胞定位:

Cytoplasm. Cell membrane.
Note: Localizes to the cytoplasm and translocates to the plasma membrane on necroptosis induction.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
亚基结构:

Homooligomer. Homotrimer; forms homotrimers on necroptosis induction. Interacts with RIPK3; the interaction is direct. Upon TNF-induced necrosis, forms in complex with PGAM5, RIPK1 and RIPK3. Within this complex, may play a role in the proper targeting of RIPK1/RIPK3 to its downstream effector PGAM5.

蛋白家族:

The protein kinase domain is catalytically inactive but contains an unusual pseudoactive site with an interaction between Lys-230 and Gln-356 residues. Upon phosphorylation by RIPK3, undergoes an active conformation (By similarity).

The coiled coil region 2 is responsible for homotrimerization.

Belongs to the protein kinase superfamily.

研究领域

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

文献引用

1). Cyclic helix B peptide alleviates proinflammatory cell death and improves functional recovery after traumatic spinal cord injury. Redox Biology (PubMed: 37290302) [IF=11.4]
2). Activation of ALDH2 attenuates high glucose induced rat cardiomyocyte fibrosis and necroptosis. Free radical biology & medicine (PubMed: 31689484) [IF=7.4]

Application: WB    Species: rat    Sample: cardiomyocytes

Fig. 8 |Changes of RIP1, RIP3 and MLKL at mRNA and protein levels in the different groups (means ± SD, n=6) A, B, C: RIP1, RIP3 and MLKL mRNA levels in cardiomyocytes normalized by GAPDH levels. **P<0.01 compared with NG; #P<0.05, ##P<0.01 compared with HG; ^P<0.05, ^^P<0.01 compared with HG+Alda-1 D: Representative western blots of RIP1, RIP3 and MLKL proteins
3). Cyclic helix B peptide promotes random‐pattern skin flap survival via TFE3‐mediated enhancement of autophagy and reduction of ROS levels. British Journal of Pharmacology (PubMed: 34622942) [IF=7.3]

Application: WB    Species: Mouse    Sample: skin tissues

FIGURE 2 CHBP inhibits necroptosis in random-pattern skin flaps. (a,b) Representative immunohistochemical staining for RIPK3 (brown) in mouse skin tissues from the control, FLAP and FLAP + CHBP groups and quantification of integrated absorbance of RIPK3 signal (n = 6 mice per group). The tissues were counterstained with haematoxylin (blue; scale bar = 100 μm). (c,d) Representative images of immunofluorescence staining of mouse skin samples (DAPI staining of the nuclei) and quantification graph for RIPK1 (green)-positive cells (n = 6 mice per group). Scale bar: 10 μm. Skin samples were harvested from mice in the control, FLAP and FLAP + CHBP groups. (e–g) CHBP treatment attenuated the activation of RIPK1, RIPK3 and MLKL induced by ischaemia–reperfusion injury. The expression of caspase 8 (CASP8) was significantly increased, which has an inhibitory effect on necroptosis. Densitometric quantification is shown (n = 6 mice per group). Data shown are means ± SEM. *P 
4). 1, 3-Dichloro-2-propanol-Induced Renal Tubular Cell Necroptosis through the ROS/RIPK3/MLKL Pathway. Journal of Agricultural and Food Chemistry (PubMed: 36000575) [IF=6.1]
5). Different cellular mechanisms from low- and high-dose zinc oxide nanoparticles-induced heart tube malformation during embryogenesis. Nanotoxicology (PubMed: 36137004) [IF=5.0]
6). Jia-Ji Electro-Acupuncture Improves Locomotor Function With Spinal Cord Injury by Regulation of Autophagy Flux and Inhibition of Necroptosis. Frontiers in Neuroscience (PubMed: 33551728) [IF=4.3]

Application: WB    Species: Rat    Sample:

FIGURE 9 Western blot results on the expression of RIPK1, RIPK3, and MLKL. (A) Expression of RIPK1 protein in each group (RIPK1/β-actin). ##P < 0.01, vs. Sham; *P ≤ 0.05, vs. Model; &&P < 0.01, &P < 0.05, vs. EA. (B) Expression of RIPK3 protein in each group (RIPK3/β-actin). ##P < 0.01, vs. Sham; *P < 0.05, vs. Model; &P < 0.05, &&P< 0.01, vs. EA. (C) Expression of MLKL protein in each group (MLKL/β-actin). ##P < 0.01, vs. Sham; *P < 0.05, **P < 0.01, vs. Model; &&P < 0.01, vs. EA.
7). 2-BFI Provides Neuroprotection Against Inflammation and Necroptosis in a Rat Model of Traumatic Brain Injury. Frontiers in Neuroscience (PubMed: 31293382) [IF=4.3]

Application: WB    Species: rat    Sample: pericontusional cortex

FIGURE 6 | The effects of 2-BFI on RIP1, RIP3, and MLKL expression after TBI. Quantitative real-time PCR analysis shows that TBI-induced RIP1 (A) and RIP3 (B)mRNA overexpression in the pericontusional cortex was inhibited by 2-BFI treatment. (C) Representative Western bands showing the protein expression of RIP1,RIP3, and their substrate MLKL in the pericontusional cortex at 72 h after TBI.
8). Alcohol induces hepatocytes necroptosis through the LC3/RIPK1/RIPK3 pathway. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association (PubMed: 37898230) [IF=4.3]
9). RIP1/RIP3/MLKL Mediates Myocardial Function Through Necroptosis in Experimental Autoimmune Myocarditis. Frontiers in Cardiovascular Medicine (PubMed: 34497836) [IF=3.6]

Application: WB    Species: Rat    Sample: myocardial tissues

Figure 3 Protein expression levels of RIP1, RIP3, and MLKL in myocardial tissues of acute and chronic stages detected by Western blot. (A) Western blot analysis of protein expression of RIP1/RIP3/MLKL in rat myocardium during “early” and “late” stages. (B–D) Quantification of RIP1 (B), RIP3 (C), MLKL (D) in (A). (E) Western blot analysis of marker protein expression of autophagosome LC-3 I and LC-3 II in rat myocardium during “early” and “late” stages. (F) Quantification of LC-3 I and LC-3 II in e. All data are presented as mean ± SEM. A Student's t-test was performed. **p < 0.05 means compared with control group (3W); *p < 0.05 means vs. control Group (8 weeks) comparison.
10). Effects of 17-AAG on the RIP1/RIP3/MLKL pathway during the development of heart failure following myocardial infarction in rats. Journal of Pharmacological Sciences (PubMed: 34384567) [IF=3.5]

Application: WB    Species: Rat    Sample: H9c2 cells

Fig. 3. Left ventricular necroptosis-regulating protein contents of the 17-AAG- or vehicle-treated CAL (C, closed column) and Sham rats (S, open column) at the 8th week after the operation. (A) Representative Western immunoblot images. (BeG) Semi-quantitative values of left ventricular phospho-RIP1 (B), RIP1 (C), phospho-RIP3 (D), RIP3 (E), phospho- MLKL (F), MLKL (G), cleaved caspase-8 (H), and TNF- a (І) contents. Each value represents the mean ± SEM of 8 animals. *p < 0.05 vs. corresponding Sham group. # p < 0.05 vs. vehicle-treated CAL group.
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