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Merck

420116

JNK Inhibitor I, (L)-Form, Cell-Permeable

The JNK Inhibitor I, (L)-Form, Cell-Permeable controls the biological activity of JNK. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

別名:

JNK Inhibitor I, (L)-Form, Cell-Permeable, c-Jun NH2-terminal kinase, SAPK Inhibitor I, (L)-JNKI1, ( L)-HIV-TAT48-57-PP-JBD20, H-GRKKRRQRRRPPRPKRPTTLNLFPQVPRSQDT-NH2

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この商品について

実験式（ヒル表記法）:
C168H293N67O42
分子量:
3923.55
NACRES:
NA.77
UNSPSC Code:
12352200

主要文書

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製品名

JNK Inhibitor I, (L)-Form, Cell-Permeable, The JNK Inhibitor I, (L)-Form, Cell-Permeable controls the biological activity of JNK. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

assay

≥97% (HPLC)

form

lyophilized solid

potency

1 μM IC50

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated (hygroscopic)

color

white

solubility

water: 2 mg/mL

shipped in

ambient

storage temp.

−20°C

Quality Level

100

関連するカテゴリー

Biochem/physiol Actions

Cell permeable: yes
Primary Target
JNK
Product does not compete with ATP.
Reversible: no

Disclaimer

Toxicity: Standard Handling (A)

General description

A cell-permeable, biologically active peptide consisting of a carboxyl terminal sequence derived from the JNK-binding domain (JBD) and an amino terminal peptide containing the HIV-TAT48-57 sequence. Blocks c-Jun NH2-terminal kinase (JNK) signaling by preventing the activation of the transcription factor c-jun (IC50 ~ 1 µM). This effect appears to be due to inhibition of phosphorylation of the activation domains of JNK. Contains the minimal 20-amino acid inhibitory domain of islet-brain (IB) that is shown to be critical for interaction with JNK linked to the 10-amino acid HIV-TAT48-57 sequence as a carrier peptide and two proline residues as spacer. Inhibits IL-1β-induced c-jun and c-fos expression in insulin secreting βTC-3 cells and offers protection against apoptosis. Does not affect insulin secretion and has no effect on either ERK 1/2 or p38 activities.

Legal Information

Sold under license of U.S. Patents 6,043,083 and 6,410,693.
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Other Notes

Barr, R.K., et al. 2002. J. Biol. Chem.277, 10987.
Bonny, C., et al. 2001. Diabetes50, 77.
H-Gly-Arg-Lys-Lys-Arg-Agr-Gln-Arg-Arg-Arg-Pro-Pro-Arg-Pro-Lys-Arg-Pro-Thr-Thr-Leu-Asn-Leu-Phe-Pro-Gln-Val-Pro-Arg-Ser-Gln-Asp-Thr-NH₂

Packaging

Packaged under inert gas

Physical form

Supplied as a trifluoroacetate salt.

Preparation Note

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

保管分類

11 - Combustible Solids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

試験成績書（COA）

製品のロット番号・バッチ番号を入力して、試験成績書（COA） を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。

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文書ライブラリで、最近購入した製品の文書を検索できます。

文書ライブラリにアクセスする

C Bonny et al.
Diabetes, 50(1), 77-82 (2001-01-09)
Stress conditions and proinflammatory cytokines activate the c-Jun NH2-terminal kinase (JNK), a member of the stress-activated group of mitogen-activated protein kinases (MAPKs). We recently demonstrated that inhibition of JNK signaling with the use of the islet-brain (IB) 1 and 2
Roberta Caruso et al.
Journal of immunology (Baltimore, Md. : 1950), 178(9), 5957-5965 (2007-04-20)
Helicobacter pylori (Hp) infection is associated with gastric inflammation and ulceration. The pathways of tissue damage in Hp-infected subjects are complex, but evidence indicates that T cell-derived cytokines enhance the synthesis of matrix metalloproteinases (MMP) that contribute to mucosal ulceration
Renae K Barr et al.
The Journal of biological chemistry, 277(13), 10987-10997 (2002-01-16)
The c-Jun N-terminal kinases (JNKs) are a subfamily of the mitogen-activated protein kinases (MAPKs). Although progress in evaluating the functions of other MAPKs has been facilitated by the characterization of specific inhibitors, no JNK-directed inhibitor is commercially available. We have
Lili Xu et al.
Immunity, 33(3), 313-325 (2010-09-28)
The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-β (TGF-β)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline
Pau Marfull-Oromí et al.
Methods in molecular biology (Clifton, N.J.), 2438, 287-301 (2022-02-12)
In vitro studies have provided valuable insights to the function and mechanisms in axon guidance. In this chapter, we will introduce the rodent "open-book" assay, pre- or postcrossing explant culture and the dissociated neuron culture. They have been used to
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グローバルトレードアイテム番号

カタログ番号GTIN
420116-1MGCN04055977187946

ライフサイエンス、有機合成、材料科学、クロマトグラフィー、分析など、あらゆる分野の研究に経験のあるメンバーがおります。.

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