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4-Amino-3-hydroxybenzoic acid

$64

  • Brand : BIOFRON

  • Catalogue Number : BN-O1160

  • Specification : 98%(HPLC)

  • CAS number : 2374-03-0

  • Formula : C7H7NO3

  • Molecular Weight : 153.14

  • PUBCHEM ID : 137566

  • Volume : 5mg

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Catalogue Number

BN-O1160

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

153.14

Appearance

Botanical Source

Structure Type

Category

SMILES

C1=CC(=C(C=C1C(=O)O)O)N

Synonyms

4-Amino-3-hydroxy benzoic acid/2-hydroxyaniline/Benzoic acid, 4-amino-3-hydroxy-/2-Amino-5-carboxyphenol/4-Amino-3-hydroxybenzoic acid/3-hydroxy-4-aminobenzoate/2hdr/2-hydroxy-4-carboxyaniline/3-hydroxy-4-amino-benzoic acid

IUPAC Name

4-amino-3-hydroxybenzoic acid

Density

1.5±0.1 g/cm3

Solubility

Flash Point

187.1±26.5 °C

Boiling Point

385.7±37.0 °C at 760 mmHg

Melting Point

211-215 °C(lit.)

InChl

InChl Key

NFPYJDZQOKCYIE-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:2374-03-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

30912765

Abstract

Acute kidney injury (AKI) can lead to chronic kidney disease (CKD) if injury is severe and/or repair is incomplete. However, the pathogenesis of CKD following renal ischemic injury is not fully understood. Capillary rarefaction and tubular hypoxia are common findings during the AKI-to-CKD transition. We investigated the tubular stress response to hypoxia and demonstrated that a stress-responsive transcription factor, FoxO3, was regulated by prolyl hydroxylase (PHD). Hypoxia inhibited FoxO3 prolyl hydroxylation and FoxO3 degradation, leading to FoxO3 accumulation and activation in tubular cells. Hypoxia-activated HIF-1α contributed to FoxO3 activation and functioned to protect kidneys, as tubular deletion of HIF-1α decreased hypoxia-induced FoxO3 activation and resulted in more severe tubular injury and interstitial fibrosis following ischemic injury. Strikingly, tubular deletion of FoxO3 during the AKI-to-CKD transition aggravated renal structural and functional damage, leading to a much more profound CKD phenotype. We show that tubular deletion of FoxO3 resulted in decreased autophagic response and increased oxidative injury, which may explain renal protection by FoxO3. Our study indicates that in the hypoxic kidney, stress-responsive transcription factors can be activated for adaptions to counteract hypoxic insults, thus attenuating CKD development.

KEYWORDS

Keywords: Cell Biology, Nephrology Keywords: Autophagy, hypoxia

Title

FoxO3 activation in hypoxic tubules prevents chronic kidney disease

Author

Ling Li,1 Huimin Kang,1,2 Qing Zhang,3 Vivette D. D’Agati,4 Qais Al-Awqati,5 and Fangming Lincorresponding author1

Publish date

2019 Jun 3;

PMID

5289873

Abstract

When a human being is placed for several days on a completely defined diet, consisting almost entirely of small molecules that are absorbed from the stomach into the blood, intestinal flora disappear because of lack of nutrition. By this technique, the composition of body fluids can be made constant (standard deviation about 10%) after a few days, permitting significant quantitative analyses to be performed. A method of temperature-programmed gas-liquid partition chromatography has been developed for this purpose. It permits the quantitative determination of about 250 substances in a sample of breath, and of about 280 substances in a sample of urine vapor. The technique should be useful in the application of the principles of orthomolecular medicine.

Title

Quantitative Analysis of Urine Vapor and Breath by Gas-Liquid Partition Chromatography

Author

Linus Pauling,* Arthur B. Robinson,* Roy Teranishi,† and Paul Cary*

Publish date

1971 Oct;

PMID

2538840

Abstract

Inbred Lewis (LEW/N) female rats develop an arthritis in response to group A streptococcal cell wall peptidoglycan polysaccharide (SCW), which mimics human rheumatoid arthritis. Histocompatible Fischer (F344/N) rats do not develop arthritis in response to the same SCW stimulus. To evaluate this difference in inflammatory reactivity, we examined the function of the hypothalamic-pituitary-adrenal (HPA) axis and its ability to modulate the development of the inflammatory response in LEW/N and F344/N rats. We have found that, in contrast to F344/N rats, LEW/N rats had markedly impaired plasma corticotropin and corticosterone responses to SCW, recombinant human interleukin 1 alpha, the serotonin agonist quipazine, and synthetic rat/human corticotropin-releasing hormone. LEW/N rats also had smaller adrenal glands and larger thymuses. Replacement doses of dexamethasone decreased the severity of LEW/N rats’ SCW-induced arthritis. Conversely, treatment of F344/N rats with the glucocorticoid receptor antagonist RU 486 or the serotonin antagonist LY53857 was associated with development of severe inflammatory disease, including arthritis, in response to SCW. These findings support the concept that susceptibility of LEW/N rats to SCW arthritis is related to defective HPA axis responsiveness to inflammatory and other stress mediators and that resistance of F344/N rats to SCW arthritis is regulated by an intact HPA axis-immune system feedback loop.

Title

Inflammatory mediator-induced hypothalamic-pituitary-adrenal axis activation is defective in streptococcal cell wall arthritis-susceptible Lewis rats.

Author

E M Sternberg, J M Hill, G P Chrousos, T Kamilaris, S J Listwak, P W Gold, and R L Wilder

Publish date

1989 Apr;


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