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MBP MAPK Substrate acetate can be used as an exogenous substrate for MAPK.

MBP (MAPK) Substrate is an exogenous substrate utilized for MAPK.

Apelin-12 acetate possesses a high affinity to orphan receptor APJ receptor. Apelin-12 acetate inhibits the JNK and p38 MAPK signaling pathway of the apoptosis-related MAPKs family, thus offering protection to neurons.

Muramyl dipeptide (MDP) is a synthetic immunoreactive peptide, consisting of N-acetyl muramic acid attached to a short amino acid chain of L-Ala-D-isoGln. It indirectly decreases osteoclast differentiation by reducing the RANKL OPG ratio and directly increases osteoblast differentiation by up-regulating Runx2 gene expression through MAPK pathways, thereby inducing bone formation via Runx2.

EGF-R (661-681) T669 Peptide, a substrate of MAPK, facilitates the measurement of MAPK catalytic activity [1].

KRas/son of sevenless 1 (SOS1) interaction inhibitor. Binds within nucleotide binding pocket of KRas (Kd values are 106 - 176 nM for wild type KRas and various KRas mutants). Inhibits nucleotide binding to KRas in a concentration dependent manner. Display

Ac2-26 acetate is an active N-terminal peptide of annexin A1(AnxA1). Ac2-26 acetate decreases AnxA1 protein expression and inhibits the activation of NF-κB and MAPK pathways in the injured lung tissue. Ac2-26 acetate attenuates ischemia-reperfusion-induced acute lung injury.

MK2-IN-5, a pseudosubstrate of Mk2 with an inhibition constant (K_i) of 8 μM, selectively targets the protein interaction domain of the MAPK pathway and inhibits the phosphorylation of HSP25 and HSP27 [1] [2] [3].

This Mitogen-activated protein kinase (MAP kinase) fragment has a peptide sequence of Lys-Tyr-Ile-His-Ser-Ala-Asn-Val-Leu. The MAP kinases are serine/threonine-specific protein kinases belonging to the CMGC (CDK/MAPK/GSK3/CLK) kinase group.

Ac2-26 TFA, an active N-terminal peptide of annexin A1 (AnxA1), attenuates ischemia-reperfusion-induced acute lung injury. Ac2-26 also decreases AnxA1 protein expression, inhibits the activation of NF-κB and MAPK pathways in the injured lung tissue.

Cyclosporin H (CsH), a specific inhibitor of FPR1, inhibited lung inflammation in the ALI models. CsH significantly attenuated MTDs or NFP-induced inflammatory lung injury and activation of MAPK and AKT pathways. Cyclosporin H is a viral transduction enha

OVA-E1 peptide TFA activates the p38 and JNK cascades similarly in mutant and wild-type thymocytes.

Amylin (AMY3) receptor antagonist. Inhibits andrenomedulin-stimulated cAMP production in vitro. Protects against oligomeric Aβ-induced increase in intracellular Ca2+, activation of PKA, MAPK, Akt and cFOS and cell death in neuronal cell culture. Blocks el