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SAB4200094

Sigma-Aldrich

Anti-PKM2 (isoform M1) antibody produced in rabbit

enhanced validation

~1.5 mg/mL, affinity isolated antibody

Synonym(s):

Anti-CTHBP, Anti-OIP3 (OPA-interacting protein 3), Anti-PK3, Anti-PKM, Anti-Pyruvate Kinase, MUSCLE (isoform M1), Anti-TCB, Anti-THBP1 (thyroid hormone-binding protein, cytosolic)

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.44

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~60 kDa

species reactivity

human, rat, mouse

enhanced validation

recombinant expression
Learn more about Antibody Enhanced Validation

concentration

~1.5 mg/mL

technique(s)

immunocytochemistry: 5-10 μg/mL using HeLa cells
immunohistochemistry: 20-30 μg/mL using formalin-fixed paraffin embedded human colon
immunoprecipitation (IP): 2-4 μg using rat brain extract (S2 fraction)
western blot: 1-2 μg/mL using mouse brain extract (S2 fraction)

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... PKM2(5315)

General description

Pyruvate Kinase (PK) is a key regulatory enzyme in glycolysis and has four known isoforms, namely, L, R, M1 and M2. The M2 isoform has been linked to cancer metastasis. PK isoform M1 is expressed during the development of the embryo and is the dominant isoform in cardiac, brain and skeletal muscle tissues.

Specificity

Anti-PKM2 (isoform M1) antibody is specific for human, mouse and rat PKM2 (Isoform M1)/PKM1. In immunoblotting, detection of the PKM2 (Isoform M1) /PKM1 band is specifically inhibited by the immunizing peptide.

Application

Anti-PKM2 (isoform M1) antibody produced in rabbit has been used in:
  • immunoblotting
  • immunoprecipitation
  • immunohistochemistry
  • immunocytochemistry

Biochem/physiol Actions

Pyruvate kinase (PK) is a key enzyme in the glycolytic pathway. Knockdown of the M2 isoform in human cancer cell lines and its replacement by the M1 isoform has been shown to lead to reversal of the Warburg effect, and reduced ability to form tumors in mouse xenografts. Phosphorylation of the M2 isoform at Tyr105 inhibits its activity and is common in human cancers, suggesting that Tyr105 is a critical metabolic switch in cancer cells that promotes tumorigenesis.

Physical form

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Cell communication and signaling : CCS, 20(1), 76-76 (2022-06-01)
Acute kidney injury (AKI) is associated with a severe decline in kidney function caused by abnormalities within the podocytes' glomerular matrix. Recently, AKI has been linked to alterations in glycolysis and the activity of glycolytic enzymes, including pyruvate kinase M2
Jianshuang Guo et al.
Frontiers in oncology, 9, 993-993 (2019-10-22)
Glioblastoma (GBM) is the most prevalent malignant tumor in the central nervous system. Aerobic glycolysis, featured with elevated glucose consumption and lactate production, confers selective advantages on GBM by utilizing nutrients to support rapid cell proliferation and tumor growth. Pyruvate
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Notch signaling critically controls cell fate decisions in mammals, both during embryogenesis and in adults. In the skeleton, Notch suppresses osteoblast differentiation and sustains bone marrow mesenchymal progenitors during postnatal life. Stabilizing mutations of Notch2 cause Hajdu-Cheney syndrome, which is

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