Mouse Angiotensinogen (AGT) Protein

Product specifications

Proteins and Peptides

Angiotensinogen (AGT)

E. coli

Mouse

Unconjugated

Molecular Weight: Calculated MW: 56.4 kDa  Observed MW (SDS-PAGE): 55 kDa
Concentration: Prior to lyophilization: 200 µg/ml
Sequence Fragment: Ala23-Val477
Tag: N-terminal His tag

Recombinant

> 90%

10 µg

50 µg

100 µg

200 µg

500 µg

Lyophilized To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex.

WB, SDS-PAGE

Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 1 mM DTT, 5% Trehalose and Proclin-300.

Shipped within 5-7 working days.

Store at 2-8 °C for up to one month. Store at -80 °C for up to one year. Avoid repeated freeze/thaw cycles.

No

P11859

ANHU,SERPINA8,hFLT1

Protein AGT

RUO

This product is for research use only.   Not for human consumption, cosmetic, therapeutic or diagnostic use.

Descripción

Angiotensinogen (AGT) is a protein primarily produced and secreted by the liver, although it is also synthesized by other tissues, including the kidney and adipose tissue. It serves as the precursor molecule for the renin-angiotensin system (RAS), a key regulatory pathway involved in blood pressure regulation, fluid balance, and electrolyte homeostasis. AGT is converted into angiotensin I by the enzyme renin, which is released by the kidneys in response to various stimuli, such as decreased blood pressure or sodium levels. Angiotensin I is further converted into angiotensin II by angiotensin-converting enzyme (ACE), leading to vasoconstriction, aldosterone release, and sodium reabsorption, ultimately raising blood pressure. Dysregulation of the RAS, including alterations in AGT levels, has been implicated in hypertension, cardiovascular disease, and kidney disorders. Therapeutic interventions targeting the RAS, such as ACE inhibitors and angiotensin receptor blockers, are commonly used to manage hypertension and related conditions. Understanding the role of AGT in the RAS provides insights into cardiovascular health and potential avenues for therapeutic intervention. Ongoing research continues to elucidate the intricate mechanisms underlying AGT regulation and its implications for human health and disease

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