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Rottlerin

$280

  • Brand : BIOFRON

  • Catalogue Number : BN-O1867

  • Specification : 98%(HPLC)

  • CAS number : 82-08-6

  • Formula : C30H28O8

  • Molecular Weight : 516.54

  • PUBCHEM ID : 5281847

  • Volume : 20mg

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Catalogue Number

BN-O1867

Analysis Method

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

516.54

Appearance

Powder

Botanical Source

Structure Type

Category

SMILES

CC1=C(C(=C(C(=C1O)C(=O)C)O)CC2=C(C3=C(C(=C2O)C(=O)C=CC4=CC=CC=C4)OC(C=C3)(C)C)O)O

Synonyms

(E)-1-[6-[(3-acetyl-2,4,6-trihydroxy-5-methylphenyl)methyl]-5,7-dihydroxy-2,2-dimethylchromen-8-yl]-3-phenylprop-2-en-1-one

IUPAC Name

Applications

Density

1.4±0.1 g/cm3

Solubility

DMSO : 2 mg/mL (3.87 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)

Flash Point

266.0±27.8 °C

Boiling Point

800.4±65.0 °C at 760 mmHg

Melting Point

200 °C

InChl

InChI=1S/C25H39NO7/c1-6-26-11-22(12-30-2)8-7-16(32-4)24-14-9-13-15(31-3)10-23(28,17(14)18(13)27)25(29,21(24)26)20(33-5)19(22)24/h13-17,19-21,28-29H,6-12H2,1-5H3

InChl Key

DEZFNHCVIZBHBI-ZHACJKMWSA-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#:82-08-6) 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

31800260

Abstract

In visceral smooth muscle cells (SMCs), the large-conductance Ca2+-activated K+ (BK) channel is one of the key elements underlying a negative feedback mechanism that is essential for the regulation of intracellular Ca2+ concentration. Although leucine-rich repeat-containing (LRRC) proteins have been identified as novel auxiliary γ-subunits of the BK channel (BKγ) in several cell types, its physiological roles in SMCs are unclear. The BKγ expression patterns in selected SM tissues were examined using real-time PCR analyses and Western blotting. The functional contribution of BKγ1 to BK channel activity was examined by whole cell patch-clamp in SMCs and heterologous expression systems. BKγ1 expression in mouse bronchial SMCs (mBSMCs) was higher than in other several SMC types. Coimmunoprecipitation and total internal reflection fluorescence imaging analyses revealed molecular interaction between BKα and BKγ1 in mBSMCs. Under voltage-clamp, steady-state activation of BK channel currents at pCa 8.0 in mBSMCs occurred in a voltage range comparable to that of reconstituted BKα/BKγ1 complex. However, this range was much more negative than in mouse aortic SMCs (mASMCs) or in HEK293 cells expressing BKα alone and β-subunit (BKβ1). Mallotoxin, a selective activator of BK channel that lacks BKγ1, dose-dependently activated BK currents in mASMCs but not in mBSMCs. The abundant expression of BKγ1 in mBSMCs extensively facilitates BK channel activity to keep the resting membrane potential at negative values and prevents contraction under physiological conditions.

KEYWORDS

BK channel; BKγ1 subunit; LRRC26; bronchus; smooth muscle cell.

Title

Roles of LRRC26 as an auxiliary γ1-subunit of large-conductance Ca 2+-activated K + channels in bronchial smooth muscle cells

Author

Sayuri Noda 1, Yoshiaki Suzuki 1, Hisao Yamamura 1, Wayne R Giles 2, Yuji Imaizumi 1

Publish date

2020 Feb 1;

PMID

31422080

Abstract

We previously demonstrated that activation of protein kinase Cδ (PKCδ) is critical for methamphetamine (MA)-induced dopaminergic toxicity. It was recognized that microsomal epoxide hydrolase (mEH) also induces dopaminergic neurotoxicity. It was demonstrated that inhibition of PKC modulates the expression of mEH. We investigated whether MA-induced PKCδ activation requires mEH induction in mice. MA treatment (8 mg/kg, i.p., × 4; 2 h interval) significantly enhanced the level of phosphorylated PKCδ in the striatum of wild type (WT) mice. Subsequently, treatment with MA resulted in significant increases in the expression of cleaved PKCδ and mEH. Treatment with MA resulted in enhanced interaction between PKCδ and mEH. PKCδ knockout mice exhibited significant attenuation of the enhanced mEH expression induced by MA. MA-induced hyperthermia, oxidative stress, proapoptotic potentials, and dopaminergic impairments were attenuated by PKCδ knockout or mEH knockout in mice. However, treating mEH knockout in mice with PKCδ inhibitor, rottlerin did not show any additive beneficial effects, indicating that mEH is a critical mediator of neurotoxic potential of PKCδ. Our results suggest that MA-induced PKCδ activation requires mEH induction as a downstream signaling pathway and that the modulation of the PKCδ and mEH interaction is important for the pharmacological intervention against MA-induced dopaminergic neurotoxicity.

KEYWORDS

Dopamine; Methamphetamine; Oxidative stress; PKCδ knockout mice; Proapoptosis; mEH knockout mice.

Title

Protein kinase Cδ mediates methamphetamine-induced dopaminergic neurotoxicity in mice via activation of microsomal epoxide hydrolase

Author

Eun-Joo Shin 1, Ji Hoon Jeong 2, Garima Sharma 1, Naveen Sharma 1, Dae-Joong Kim 3, Duc Toan Pham 1, Quynh Dieu Trinh 1, Duy-Khanh Dang 4, Seung-Yeol Nah 5, Guoying Bing 6, Hyoung-Chun Kim 7

Publish date

2019 Nov

PMID

31408224

Abstract

Rottlerin is a cytostatic and cytotoxic drug in a variety of cancer cells. Our previous experience demonstrated that depending upon the genetic/biochemical background of cancer cells, rottlerin is able to induce both apoptotic and autophagic cell death, or dramatically disturb protein homeostasis leading to lethal cellular atrophy. In the current study, we investigated the cytotoxic effects and mechanisms of rottlerin against human amelanotic A375 melanoma cells. In this cell line, rottlerin exhibits its main and newest cytotoxic properties, that is, growth arrest, apoptosis induction, and translation shutoff. In fact, the drug, time-, and dose-dependently, markedly inhibited cell proliferation through cyclin D1 downregulation and induced apoptotic cell death as early as after 18 h treatment. Mechanistically, rottlerin triggered apoptosis by both intrinsic and extrinsic pathways. Both pathways are likely activated by the downregulation of the antiapoptotic B-cell lymphoma 2 (Bcl-2) protein, which simultaneously affects mitochondrial and endoplasmic reticulum (ER) membranes stability. Concomitantly to extrinsic apoptosis induction, the rottlerin-activated ER stress/eukaryotic initiation factor 2 (eIF2) α axis blocked the translational apparatus. The altered proteostasis precluded the complete cells’ rescue from death in the presence of apoptosis inhibitors.

KEYWORDS

ER stress; apoptosis; melanoma; mitochondria; protein synthesis; rottlerin.

Title

Multiple mechanisms of Rottlerin toxicity in A375 melanoma cells

Author

Francesca Ietta 1, Giuseppe Valacchi 2 3 4, Linda Benincasa 1, Alessandra Pecorelli 3, Laura Cresti 1, Emanuela Maioli 1

Publish date

2019 Nov;