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SRP6257

Sigma-Aldrich

ADIPOQ/Adiponectin/ACRP30 human

recombinant, expressed in HEK 293 cells, ≥92% (SDS-PAGE)

Synonym(s):

ACDC, ACRP30, ADIPOQ, APM1, Adiponectin, GBP28

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About This Item

UNSPSC Code:
12352202
NACRES:
NA.32
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biological source

human

recombinant

expressed in HEK 293 cells

tag

6-His tagged (C-terminus)

Assay

≥92% (SDS-PAGE)

form

lyophilized powder

mol wt

calculated mol wt 25.4 kDa
observed mol wt 28-33 kDa (DTT-reduced. Protein migrates due to glycosylation. Glu 19 is the predicted N-terminus.)

packaging

pkg of 10 μg

impurities

<1 EU/μg endotoxin (LAL test)

UniProt accession no.

shipped in

wet ice

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certified reference material, pharmaceutical secondary standard

application(s)

pharmaceutical small molecule

application(s)

pharmaceutical small molecule

application(s)

pharmaceutical small molecule

application(s)

pharmaceutical small molecule

form

liquid

form

liquid

form

liquid

form

-

vapor pressure

760 mmHg ( 109 °C)

vapor pressure

88 mmHg ( 20 °C)

vapor pressure

10 mmHg ( 39 °C)

vapor pressure

120 mmHg ( 20 °C)

packaging

pkg of 1 mL

packaging

pkg of 1 mL

packaging

pkg of 1 mL

packaging

pkg of 20 mL

refractive index

n20/D 1.438 (lit.)

refractive index

n20/D 1.395 (lit.)

refractive index

n20/D 1.401 (lit.)

refractive index

n20/D 1.367 (lit.)

General description

Adiponectin (also called Acrp30, AdipoQ) is an adipocyte specific secreted protein that circulates in the plasma. It is induced during adipocyte differentiation and its secretion is stimulated by insulin.[1][2] The protein has a carboxyl-terminal globular domain and an amino-terminal collagen domain.[3] The gene is mapped to human chromosome 3q27.[4]

Biochem/physiol Actions

Adiponectin (ADIPOQ) has anti-atherosclerotic and anti-inflammatory properties.[5] ADIPOQ has a role in physiological processes such as energy homeostasis and obesity.[1][2] It exhibits anti-diabetic action by interacting with adiponectin receptors, AdipoR1 and AdipoR2.[3] Low levels of adiponectin are also linked with hypertension and dyslipidemia.[2] Mutation in the gene encoding it is linked with risk for endometrial cancer.[6]

Physical form

Lyophilized from 0.22 μm filtered solution in PBS. Generally 5-8% Mannitol or trehalose is added as a protectant before lyophilization.

Reconstitution

Centrifuge the vial prior to opening. Reconstitute in sterile PBS, pH 7.4 to a concentration of 50 μg/mL. Do not vortex. This solution can be stored at 2-8°C for up to 1 month. For extended storage, it is recommended to store at -20°C.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Francesca Raimondo et al.
Proteomes, 8(2) (2020-05-14)
Renal tubular cells release urinary extracellular vesicles (uEV) that are considered a promising source of molecular markers for renal dysfunction and injury. We investigated uEV proteomes of patients with hereditary salt-losing tubulopathies (SLTs), focusing on those caused by Gitelman and
Xiangzhu Zhu et al.
The Journal of nutrition, 144(11), 1734-1741 (2014-08-29)
The kidney-specific sodium-potassium-chloride cotransporter (NKCC2) protein encoded by solute carrier family 12 member 1 (SLC12A1) is the direct downstream effector of the inward-rectifier potassium channel (ROMK) encoded by potassium inwardly-rectifying channel, subfamily J, member 1 (KCNJ1), both of which are
Monica Carmosino et al.
Biology of the cell, 104(4), 201-212 (2012-01-04)
The central role of Na+-K+-2Cl- cotransporter type 2 (NKCC2) in vectorial transepithelial salt reabsorption in thick ascending limb cells from Henle's loop in the kidney is evidenced by the effects of loop diuretics, the pharmacological inhibitors of NKCC2, that are
Michelle Y Monette et al.
American journal of physiology. Renal physiology, 300(4), F840-F847 (2011-01-07)
The Na-K-Cl cotransporter (NKCC2) is the major salt transport pathway in the thick ascending limb of Henle's loop and is part of the molecular mechanism for blood pressure regulation. Recent screening of ∼3,000 members of the Framingham Heart Study identified

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