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Thapsigargin

$1,024

  • Brand : BIOFRON

  • Catalogue Number : BN-O1865

  • Specification : 98%(HPLC)

  • CAS number : 67526-95-8

  • Formula : C34H50O12

  • Molecular Weight : 650.76

  • PUBCHEM ID : 446378

  • Volume : 20mg

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Catalogue Number

BN-O1865

Analysis Method

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

650.76

Appearance

Powder

Botanical Source

Structure Type

Category

SMILES

CCCCCCCC(=O)OC1C2C(=C(C1OC(=O)C(=CC)C)C)C3C(C(CC2(C)OC(=O)C)OC(=O)CCC)(C(C(=O)O3)(C)O)O

Synonyms

IUPAC Name

Applications

Density

1.2±0.1 g/cm3

Solubility

DMSO : 250 mg/mL (384.17 mM; Need ultrasonic)

Flash Point

209.0±25.0 °C

Boiling Point

699.6±55.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

IXFPJGBNCFXKPI-FSIHEZPISA-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#:67526-95-8) 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

32040528

Abstract

Recent studies indicated that intramammary administration of active vitamin D3 hormone (1,25D3) inhibits the inflammatory process associated with mastitis. We hypothesized that attenuation of endoplasmic reticulum (ER) stress by 1,25D3 in mammary epithelial cells (MECs) is an important cellular mechanism contributing to this beneficial effect of intramammary treatment with 1,25D3. To test this hypothesis, the effect of 1,25D3 was studied on induction of ER stress in a transformed human MEC line, MCF-7 cells. Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P < 0.05). Treatment with 1,25D3 (100 nM) inhibited TG (10 nM)- and TM (1 μg/mL)-induced mRNA and/or protein levels of ATF4, ATF6, DDIT3 and HSPA5 in MCF-7 cells (P < 0.05). In addition, 1,25D3 (100 nM) antagonized the effect of TG (10 nM) and TM (1 μg/mL) on mRNA and protein levels of VDR and mRNA levels of genes involved in production and degradation of 1,25D3 in MCF-7 cells (P < 0.05). Moreover, 1,25D3 (100 nM) inhibited nuclear factor-κB (NF-κB) activation in response to TM (10 nM) and TG (1 μg/mL) in MCF-7 cells. In conclusion, the present findings show that 1,25D3 is effective in attenuating ER stress and the NF-κB-driven inflammatory response in MCF-7 cells. This indicates that attenuation of ER stress by 1,25D3 in MECs may contribute to the recently observed inhibitory effect of intramammary treatment of dairy cows with 1,25D3 on the inflammatory process associated with mastitis.

Title

1,25-hydroxyvitamin D3 decreases endoplasmic reticulum stress-induced inflammatory response in mammary epithelial cells

Author

Gaiping Wen 1, Klaus Eder 1, Robert Ringseis 1

Publish date

2020 Feb 10;

PMID

31924446

Abstract

Recent interest in astrocyte activation states has raised the fundamental question of how these cells, normally essential for synapse and neuronal maintenance, become pathogenic. Here, we show that activation of the unfolded protein response (UPR), specifically phosphorylated protein kinase R-like endoplasmic reticulum (ER) kinase (PERK-P) signaling-a pathway that is widely dysregulated in neurodegenerative diseases-generates a distinct reactivity state in astrocytes that alters the astrocytic secretome, leading to loss of synaptogenic function in vitro. Further, we establish that the same PERK-P-dependent astrocyte reactivity state is harmful to neurons in vivo in mice with prion neurodegeneration. Critically, targeting this signaling exclusively in astrocytes during prion disease is alone sufficient to prevent neuronal loss and significantly prolongs survival. Thus, the astrocyte reactivity state resulting from UPR over-activation is a distinct pathogenic mechanism that can by itself be effectively targeted for neuroprotection.

KEYWORDS

LCN2; PERK signalling; astrocyte reactivity state; astrocytes; neurodegeneration; neuroprotection; secretome; synapse; translational neuroscience; unfolded protein response.

Title

Astrocyte Unfolded Protein Response Induces a Specific Reactivity State that Causes Non-Cell-Autonomous Neuronal Degeneration

Author

Heather L Smith 1, Oliver J Freeman 1, Adrian J Butcher 1, Staffan Holmqvist 2, Ibrahim Humoud 1, Tobias Schatzl 1, Daniel T Hughes 1, Nicholas C Verity 3, Dean P Swinden 1, Joseph Hayes 1, Lis de Weerd 1, David H Rowitch 2, Robin J M Franklin 2, Giovanna R Mallucci 4

Publish date

2020 Mar 4

PMID

31913694

Abstract

We studied the mechanisms by which carotid body glomus (type 1) cells produce spontaneous Ca2+ oscillations in normoxia and hypoxia. In cells perfused with normoxic solution at 37°C, we observed relatively uniform, low-frequency Ca2+ oscillations in >60% of cells, with each cell showing its own intrinsic frequency and amplitude. The mean frequency and amplitude of Ca2+ oscillations were 0.6 ± 0.1 Hz and 180 ± 42 nM, respectively. The duration of each Ca2+ oscillation ranged from 14 to 26 s (mean of ∼20 s). Inhibition of inositol (1,4,5)-trisphosphate receptor and store-operated Ca2+ entry (SOCE) using 2-APB abolished Ca2+ oscillations. Inhibition of endoplasmic reticulum Ca2+-ATPase (SERCA) using thapsigargin abolished Ca2+ oscillations. ML-9, an inhibitor of STIM1 translocation, also strongly reduced Ca2+ oscillations. Inhibitors of L- and T-type Ca2+ channels (Cav; verapamil>nifedipine>TTA-P2) markedly reduced the frequency of Ca2+ oscillations. Thus, Ca2+ oscillations observed in normoxia were caused by cyclical Ca2+ fluxes at the ER, which was supported by Ca2+ influx via Ca2+ channels. Hypoxia (2-5% O2) increased the frequency and amplitude of Ca2+ oscillations, and Cav inhibitors (verapamil>nifedipine>>TTA-P2) reduced these effects of hypoxia. Our study shows that Ca2+ oscillations represent the basic Ca2+ signaling mechanism in normoxia and hypoxia in CB glomus cells.

KEYWORDS

Ca2+ channel; Ca2+ oscillations; carotid body type 1 cells; frequency; mild hypoxia.

Title

Ca 2+ oscillations in rat carotid body type 1 cells in normoxia and hypoxia

Author

Donghee Kim 1, James O Hogan 1, Carl White 1

Publish date

2020 Feb 1;