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SAB3500122

Sigma-Aldrich

Monoclonal Anti-PD-1 antibody produced in mouse

clone 7A11B1, purified immunoglobulin, buffered aqueous solution

Synonym(s):

Anti-CD279, Anti-PDCD-1, Anti-Programmed cell death 1

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

7A11B1, monoclonal

form

buffered aqueous solution

species reactivity

mouse, human, rat

technique(s)

immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... PDCD1(5133)

General description

Programmed cell death 1 protein (PDCD1) is mapped to human chromosome 2q37.3. PDCD1 belongs to the Cluster of Differentiation 28 (CD28) family of receptors and has an immunoinhibitory domain. It is expressed in T and B lymphocytes.

Immunogen

raised against an ~150 amino acid recombinant protein from near the terminus terminus of mouse PD-1.

Biochem/physiol Actions

Programmed cell death 1 protein (PDCD1) modulates lymphocyte activation. Single nucleotide polymorphisms in PDCD1 is implicated in systemic lupus erythematosus, an autoimmune inflammatory disease.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Target description

Cell-mediated immune responses are initiated by T lymphocytes that are themselves stimulated by cognate peptides bound to MHC molecules on antig en-presenting cells (APC). T-cell activation is generally self-limited as activated T cells express receptors such as PD-1 (also known as PDCD-1) that mediate inhibitory signals from the APC. PD-1 can bind two different but related ligands, PDL-1 and PDL-2. Upon binding to either of these ligands, signals generated by PD-1 inhibit the activation of the immune response in the absence of "danger signals" such as LPS or other molecules associated with bacteria or other pathogens. Evidence for this is seen in PD1-null mice who exhibit hyperactivated immune systems and autoimmune diseases. Despite its predicted molecular weight, PD-1 often migrates at higher molecular weight in SDS-PAGE.

Physical form

Supplied at approx. 1 mg/mL in phosphate buffered saline containing 0.02% 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

WGK

WGK 2

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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Association of PDCD1 with susceptibility to systemic lupus erythematosus: evidence of population-specific effects
Ferreiros-Vidal I, et al.
Arthritis and Rheumatism, 50(8), 2590-2597 (2004)
Ruizhi Geng et al.
International journal of molecular sciences, 23(10) (2022-05-29)
Bladder cancer is the most cost-intensive cancer due to high recurrence rates and long follow-up times. Bladder cancer organoids were considered interesting tools for investigating better methods for the detection and treatment of this cancer. Organoids were generated from urothelial
A regulatory polymorphism in PDCD1 is associated with susceptibility to systemic lupus erythematosus in humans.
Prokunina L
Nature Genetics, 32(4), 666-669 (2002)
Nicole A Braun et al.
American journal of respiratory and critical care medicine, 190(5), 560-571 (2014-07-30)
Effective therapeutic interventions for chronic, idiopathic lung diseases remain elusive. Normalized T-cell function is an important contributor to spontaneous resolution of pulmonary sarcoidosis. Up-regulation of inhibitor receptors, such as programmed death-1 (PD-1) and its ligand, PD-L1, are important inhibitors of

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