SAB3500346
Anti-ACE2 antibody produced in rabbit
affinity isolated antibody, buffered aqueous solution
Synonym(s):
Anti-ACE2
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About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
Pricing and availability is not currently available.
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
species reactivity
mouse, human
technique(s)
immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... ACE2(59272)
General description
Angiotensin-converting enzyme-2 (ACE2), is a membrane-associated and secreted enzyme, encoded by the gene mapped to human chromosome Xp22.2. Ace 2 is a human homolog of ACE and is expressed mainly on vascular endothelium of heart, kidney, and testis. Ace2 structure comprises a N-terminal PD and a C-terminal collectrin-like domain (CLD).
Immunogen
ACE2 antibody was raised against a synthetic peptide corresponding to amino acids near the center of human ACE2.
Biochem/physiol Actions
Angiotensin-converting enzyme-2 (ACE2) catalyzes the conversion of Ang I to Ang1-9. It might also be involved in maintaining the balance of local renin-angiotensin system (RAS) in heart and kidney. Ace 2 acts as a functional receptor for spike glycoprotein of severe acute respiratory syndrome-coronavirus (SARS-CoV) and the new coronavirus (SARS-CoV-2), which is a causative agent for coronavirus disease 2019 (COVID-19). Downregulated expression of Ace 2 causes cardiovascular diseases.
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.
Linkage
The action of this antibody can be blocked using blocking peptide SBP3500346.
Physical form
Supplied in PBS with 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
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Lin Wang et al.
Theranostics, 11(2), 649-664 (2021-01-05)
The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a worldwide epidemic of the lethal respiratory coronavirus disease (COVID-19), necessitating urgent development of specific and effective therapeutic tools. Among several therapeutic targets of coronaviruses, the spike protein is
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While having already killed more than 7 million of people worldwide in 4 years, SARS-CoV-2, the etiological agent of COVID-19, is still circulating and evolving. Understanding the pathogenesis of the virus is of capital importance. It was shown that in
Elisa Avolio et al.
Clinical science (London, England : 1979), 135(24), 2667-2689 (2021-11-23)
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a broad range of clinical responses including prominent microvascular damage. The capacity of SARS-CoV-2 to infect vascular cells is still debated. Additionally, the SARS-CoV-2 Spike (S) protein may act as a
Shine Varghese Jancy et al.
Biological procedures online, 25(1), 22-22 (2023-07-27)
The entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into the host cell is mediated through the binding of the SARS-CoV-2 Spike protein via the receptor binding domain (RBD) to human angiotensin-converting enzyme 2 (hACE2). Identifying compounds that inhibit
Lai-Keng Loi et al.
Heliyon, 9(12), e22614-e22614 (2023-12-18)
The entry of SARS-CoV-2 into host cells involves the interaction between the viral spike protein and the human angiotensin-converting enzyme 2 (ACE2) receptor. Given that the spike protein evolves rapidly to evade host immunity, therapeutics that block ACE2 accessibility, such
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