Product: PDK4 Antibody
Catalog: DF7169
Description: Rabbit polyclonal antibody to PDK4
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken
Mol.Wt.: 46kDa; 46kD(Calculated).
Uniprot: Q16654
RRID: AB_2839121

View similar products>>

   Size Price Inventory
 100ul $280 In stock
 200ul $350 In stock

Lead Time: Same day delivery

For pricing and ordering contact:
Local distributors

Product Info

Source:
Rabbit
Application:
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: 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.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(90%), Zebrafish(80%), Bovine(80%), Horse(100%), Sheep(80%), Rabbit(100%), Dog(90%), Chicken(80%)
Clonality:
Polyclonal
Specificity:
PDK4 Antibody detects endogenous levels of total PDK4.
RRID:
AB_2839121
Cite Format: Affinity Biosciences Cat# DF7169, RRID:AB_2839121.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

[Pyruvate dehydrogenase [lipoamide]] kinase isozyme 4; FLJ40832; mitochondrial; Pdk4; PDK4_HUMAN; Pyruvate dehydrogenase [lipoamide] kinase isozyme 4 mitochondrial; Pyruvate dehydrogenase kinase 4; Pyruvate dehydrogenase kinase isoenzyme 4; Pyruvate dehydrogenase kinase isoform 4; Pyruvate dehydrogenase kinase isozyme 4; Pyruvate dehydrogenase kinase isozyme 4 mitochondrial;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
Q16654 PDK4_HUMAN:

Ubiquitous; highest levels of expression in heart and skeletal muscle.

Description:
This gene is a member of the PDK/BCKDK protein kinase family and encodes a mitochondrial protein with a histidine kinase domain. This protein is located in the matrix of the mitrochondria and inhibits the pyruvate dehydrogenase complex by phosphorylating one of its subunits, thereby contributing to the regulation of glucose metabolism. Expression of this gene is regulated by glucocorticoids, retinoic acid and insulin.
Sequence:
MKAARFVLRSAGSLNGAGLVPREVEHFSRYSPSPLSMKQLLDFGSENACERTSFAFLRQELPVRLANILKEIDILPTQLVNTSSVQLVKSWYIQSLMDLVEFHEKSPDDQKALSDFVDTLIKVRNRHHNVVPTMAQGIIEYKDACTVDPVTNQNLQYFLDRFYMNRISTRMLMNQHILIFSDSQTGNPSHIGSIDPNCDVVAVVQDAFECSRMLCDQYYLSSPELKLTQVNGKFPDQPIHIVYVPSHLHHMLFELFKNAMRATVEHQENQPSLTPIEVIVVLGKEDLTIKISDRGGGVPLRIIDRLFSYTYSTAPTPVMDNSRNAPLAGFGYGLPISRLYAKYFQGDLNLYSLSGYGTDAIIYLKALSSESIEKLPVFNKSAFKHYQMSSEADDWCIPSREPKNLAKEVAM

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Rabbit
100
Horse
100
Pig
90
Dog
90
Bovine
80
Sheep
80
Zebrafish
80
Chicken
80
Xenopus
60
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q16654 As Substrate

Site PTM Type Enzyme
S10 Phosphorylation
S13 Phosphorylation
K111 Ubiquitination
K122 Ubiquitination
S368 Phosphorylation
S369 Phosphorylation
K374 Ubiquitination
S381 Phosphorylation

PTMs - Q16654 As Enzyme

Substrate Site Source
P08559-1 (PDHA1) S293 Uniprot
P08559-1 (PDHA1) S300 Uniprot
P29803 (PDHA2) S291 Uniprot
P29803 (PDHA2) S298 Uniprot

Research Backgrounds

Function:

Kinase that plays a key role in regulation of glucose and fatty acid metabolism and homeostasis via phosphorylation of the pyruvate dehydrogenase subunits PDHA1 and PDHA2. This inhibits pyruvate dehydrogenase activity, and thereby regulates metabolite flux through the tricarboxylic acid cycle, down-regulates aerobic respiration and inhibits the formation of acetyl-coenzyme A from pyruvate. Inhibition of pyruvate dehydrogenase decreases glucose utilization and increases fat metabolism in response to prolonged fasting and starvation. Plays an important role in maintaining normal blood glucose levels under starvation, and is involved in the insulin signaling cascade. Via its regulation of pyruvate dehydrogenase activity, plays an important role in maintaining normal blood pH and in preventing the accumulation of ketone bodies under starvation. In the fed state, mediates cellular responses to glucose levels and to a high-fat diet. Regulates both fatty acid oxidation and de novo fatty acid biosynthesis. Plays a role in the generation of reactive oxygen species. Protects detached epithelial cells against anoikis. Plays a role in cell proliferation via its role in regulating carbohydrate and fatty acid metabolism.

Subcellular Location:

Mitochondrion matrix.

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

Ubiquitous; highest levels of expression in heart and skeletal muscle.

Subunit Structure:

Homodimer. Interacts with the pyruvate dehydrogenase complex subunit DLAT, and is part of the multimeric pyruvate dehydrogenase complex that contains multiple copies of pyruvate dehydrogenase (E1), dihydrolipoamide acetyltransferase (DLAT, E2) and lipoamide dehydrogenase (DLD, E3).

Family&Domains:

Belongs to the PDK/BCKDK protein kinase family.

References

1). An effective sodium-dependent glucose transporter 2 inhibition, canagliflozin, prevents development of hypertensive heart failure in dahl salt-sensitive rats. Frontiers in Pharmacology, 2022 (PubMed: 35370704) [IF=5.6]

Application: WB    Species: Rat    Sample:

FIGURE 6 Effect of CANA on the cardiac protein expression. (A) Heat map of individual genes within selected pathways, colored by the log2fold change; (B) Selected genes (Acadsb, Ndufb4, Pdk4, Acox1, Bdh1, and Ehhadh) were validated by Western blotting; (C,D) Quantitative evaluation of the protein expression of selected genes (Acadsb, Ndufb4, Pdk4, Acox1, Bdh1, and Ehhadh). * p < 0.05, ** p < 0.01 vs. NSD. # p < 0.05 vs. HSD.

2). Pyruvate dehydrogenase kinase 4‐mediated metabolic reprogramming is involved in rituximab resistance in diffuse large B‐cell lymphoma by affecting the expression of MS4A1/CD20. CANCER SCIENCE, 2021 (PubMed: 34252986) [IF=4.5]

Application: IF/ICC    Species: Human    Sample: DLBCL cells

FIGURE 4 Pyruvate dehydrogenase kinase 4 (PDK4) has a negative regulatory effect on MS4A1/CD20 expression in diffuse large B- cell lymphoma cells. A, B, Real- time quantitative PCR analysis of PDK4 and MS4A1 mRNA expression in U2932 and OCI- Ly8 cells transfected with PDK4 overexpressing (PDK4 OE) plasmid or empty vector (EV). C, D, CD20 (green) molecules in the plasma membrane showed a reduction after PDK4 overexpression in both U2932 and OCI- Ly8 cells. Scale bar, 15 μm. E, F, Western blot analysis of PDK4 and CD20 protein levels in U2932 and OCI- Ly8 cells with PDK4 shRNA interference or transfected with PDK4 OE plasmid or EV. *P < .05, **P < .01, ***P < .001

Application: WB    Species: Human    Sample: DLBCL cells

FIGURE 2 High pyruvate dehydrogenase kinase 4 (PDK4) is associated with rituximab (RTX) resistance and low MS4A1/CD20 in diffuse large B- cell lymphoma (DLBCL) cells. A, B, Real- time quantitative PCR analysis of PDK4 and MS4A1 mRNA expression in DLBCL cell lines U2932, OCI- ly7, and OCI- ly8. C, Western blot analysis of PDK4 and CD20 protein levels in DLBCL cell lines U2932, OCI- ly7, and OCI- ly8. D, E, Annexin V- phycoerythrin (PE)/7- AAD double staining analysis of the three DLBCL cell lines treated with RTX (50 μg/mL). F, G, Mitochondrial membrane potential of DLBCL cells following treatment with RTX for 48 hours and stained with JC- 1 probe. Representative pictures of JC- 1 staining are shown. Scale bar, 25 μm. ***P < .001

3). Abrogating PDK4 activates autophagy-dependent ferroptosis in breast cancer via ASK1/JNK pathway. Journal of cancer research and clinical oncology, 2024 (PubMed: 38678126) [IF=2.7]

4). PDK4-Mediated Metabolic Reprogramming Promotes Rituximab Resistance in Diffuse Large B-Cell Lymphoma Via Negative Regulation of MS4A1/CD20. Research Square, 2021

Application: WB    Species: Human    Sample: DLBCL cells

Figure 1. High PDK4 is associated with R-CHOP resistance in DLBCL cells. A, Gene expression detected by RNA-Seq and expression of PDK4 in DLBCL patients. Hierarchical cluster analysis of the top 11 deregulated genes in R-CHOP-sensitive patients (n = 4) and R-CHOP-resistance patients (n = 3). Upregulated genes are shown in red and downregulated genes are shown in blue. B, In the 56 cases of DLBCL cohort, PDK4 mRNA expression between GCB-DLBCL (n = 30) and ABC-DLCBL (n = 26) subtypes (* P

Application: IF/ICC    Species: Human    Sample: DLBCL cells

Figure 1. High PDK4 is associated with R-CHOP resistance in DLBCL cells. A, Gene expression detected by RNA-Seq and expression of PDK4 in DLBCL patients. Hierarchical cluster analysis of the top 11 deregulated genes in R-CHOP-sensitive patients (n = 4) and R-CHOP-resistance patients (n = 3). Upregulated genes are shown in red and downregulated genes are shown in blue. B, In the 56 cases of DLBCL cohort, PDK4 mRNA expression between GCB-DLBCL (n = 30) and ABC-DLCBL (n = 26) subtypes (* P

5). Farnesoid X Receptor Deficiency Induces Hepatic Lipid and Glucose Metabolism Disorder via Regulation of Pyruvate Dehydrogenase Kinase 4. Oxidative medicine and cellular longevity, 2022 (PubMed: 35251469)

Application: WB    Species: Mouse    Sample:

Figure 2 FXR deficiency increased hepatocyte lipid deposition and glucose metabolism and accelerated deterioration of hepatic steatosis in FXR-null mice. (a) A high-fat diet and FXR deficiency increased hepatocyte lipid deposition. PV: portal vein. Upper panel: bar, 200 μm, representative images H&E staining of liver tissues; middle panel: bar, 200 μm, lower panel: bar, 50 μm; both of them representative images of Oil Red O staining of liver tissues; WT: n = 3, KO: n = 3. SD: standard chow diet, HFD: high-fat diet. (b, c) FXR deficiency increased hepatic TG and FFA level, n = 10. (d) Relative mRNA levels of PDK4 and relevant glycolytic and lipogenic genes in the livers of FXR-null and WT control mice deal with the high-fat diet, HFD-WT: n = 3, HFD-KO: n = 3. (e) Detection expression of Scd1, PDK4, Srebp-1c, Acly, Acc1,CD36, Fasn, Gck, and tubulin. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗∗P < 0.0001.

Restrictive clause

 

Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.