phosphorylation

H1-7 (histone H1 phosphorylation site), a synthetic polypeptide serving as a PKA substrate, demonstrates utility in PKA substrate applications [1] [2].

Prosaptide TX14(A) acetate is a potent GPR37L1 and GPR37 agonist. Prosaptide Tx14(A) TFA increases both ERK1 and ERK2 phosphorylation in Schwann cells.

CREBtide acetate is a synthetic substrate for PKA (Km=3.9 μM), which is based on the phosphorylation sequence in d-CREB (cAMP response element binding protein).

RR-src acetate is a synthetic peptide derived from the amino acid sequence surrounding the phosphorylation site in pp60src.

AMARA peptide acetate is a substrate for SIK and AMPK.AMARA peptide is a minimal substrate of several members of the protein kinases family. It consists of the phosphorylation site for AMP-activated Protein Kinase (AMPK).

AY 77 (Unk-Cha-Chg-NH2) is a potent and selective PAR2 agonist. AY 77 showed selectivity for Ca2+ and ERK1/2 signaling (ec50 value of Ca2+ release was 40 nM and ec50 value of ERK1/2 phosphorylation was 2 μM). AY 77 can promote migration of human breast cancer cells in vitro.

SDKPDMAEIEKFDKSK acetate is a thymosin β4 derivative. Thymosin β4 inhibits PDGF-BB-induced fibrogenesis, proliferation and migration of HSC by blocking Akt phosphorylation.

pp60 (v-SRC) Autophosphorylation Site, Phosphorylated is a phosphorylated peptide derived from an EGFR substrate. It serves as a valuable tool for quantifying phosphorylated substrates in screening EGFR Kinase inhibitors.

Valinomycin (NSC-122023) is a cyclic depsipeptide antibiotic and a potassium-specific ionophore.Valinomycin induces PINK1 activation and promotes Parkin phosphorylation at Ser65.

Cyclo(Phe-Ala-Gly-Arg-Arg-Arg-Gly-AEEAc) is a potential nonhormonal male contraceptive that functions through the inhibition of GRTH/DDX25 phosphorylation.

Antagonist of 14.3.3 proteins (KD ≈80 nM). Competitively inhibits 14.3.3-ligand interactions without requiring phosphorylation. Blocks the ability of 14.3.3 to bind to target proteins such as Raf-1, Bad, ASK1 and exoenzyme S.

APTSTAT3-9R acetate is a selective peptide binding STAT3 with antiproliferative and antitumor activity. APTSTAT3-9R acetate and inhibits STAT3 activation and downstream signaling by specifically blocking STAT3 phosphorylation.

Potent GPR37L1 and GPR37 agonist (EC50 values are 5 and 7 nM, respectively). Stimulates signaling through pertussis toxin-sensitive G proteins. Stimulates ERK phosphorylation. Protects against cellular stress. Promotes myelin lipid synthesis and prolongs

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].

LXW7 TFA, a cyclic peptide encompassing Arg-Gly-Asp (RGD), serves as an inhibitor of integrin αvβ3. It demonstrates high binding affinity towards αvβ3 integrin, evidenced by an IC50 value of 0.68 μM. Additionally, LXW7 TFA promotes the phosphorylation of VEGFR-2 and the activation of ERK1/2, contributing to its anti-inflammatory effects [1] [2] [3].

Apelin biased agonist; exhibits bias for the G protein pathway. Stimulates endothelial NOS phosphorylation and expression, promotes proliferation, and attenuates apoptosis of human pulmonary arterial endothelial cells in vitro. Shows positive inotropic an

TCS 183 can mimic the Akt phosphorylation site on GSK3β preventing conditioning of LTD.

Prosaptide Tx14(A) TFA is a prosaposin-derived peptide and a potent agonist of both GPR37L1 and GPR37, exhibiting EC50 values of 5 nM and 7 nM, respectively. In Schwann cells, this compound enhances phosphorylation of both ERK1 and ERK2 [1] [2].

Competitive inhibitor of cGMP-dependent protein kinase (PKG); analog of a substrate peptide corresponding to a phosphorylation site of histone H2B. Competes with synthetic substrates (Ki = 86 mM) but does not inhibit phosphorylation of intact histones by

TAT-JIP effectively inhibits the phosphorylation of endogenous c-jun, which is activated by PHA–PMA [1].

TAT-DEF-Elk-1 TFA (TDE TFA) is a cell-penetrating peptide that inhibits Elk-1 by mimicking its DEF domain and disrupting its function. It effectively blocks Elk-1 phosphorylation and its subsequent nuclear translocation, without affecting the activation of ERK or MSK1. This compound serves as a valuable tool for investigating Elk-1's involvement in the development of neuronal plasticity [1].

Phosphorylated p60c-src substrate II is a pentapeptide and a phosphorylated polypeptide form of p60c-src substrate II. Phosphorylation is a critical post-translational modification (post-translationmodification) vital for biological regulatory processes [1].

DT-2 serves as a potent, selective inhibitor of cGMP-dependent protein kinase (PKG), with a Ki of 12.5 nM, effectively hindering PKG-catalyzed phosphorylation [1].

eNOS pT495 decoy peptide specifically inhibits T495 phosphorylation, thereby reducing eNOS uncoupling and mitochondrial redistribution. It is utilized in research on ventilator-induced lung injury [1].

[pTyr5] EGFR (988-993) is a compound obtained from the auto-phosphorylation site, Tyr992, located within the sequence of the epidermal growth factor receptor (EGFR 988-993). This compound is frequently found bound with the catalytically inactive protein-tyrosine phosphate 1B (PTP1B).

AMARA peptide is a substrate for SIK and AMPK.AMARA peptide is a minimal substrate of several members of the protein kinases family. It consists of the phosphorylation site for AMP-activated Protein Kinase (AMPK).

Epsilon-V1-2, a Cys-conjugated, is a biologically active peptide known as the εPKC-specific inhibitor. It hampers εPKC functionality by obstructing its translocation and the phosphorylation of MARCKS, additionally perturbing εPKC's interaction with its anchoring protein, εRACK. The peptide includes a cysteine residue at its C-terminus, facilitating the formation of potential disulfide bonds with carrier proteins. Pyroglutamyl formation can occur spontaneously at the N-terminus if glutamine or glutamic acid is present, enhancing peptide stability against gastrointestinal proteases. Pyroglutamyl peptides, a recognized subset, are accounted for in the peptide's purity during HPLC analysis.

N-Oleoyl-L-Serine (N-Oleoylserine) is an endogenous long-chain fatty acid amide that is a lipid modulator of bone remodeling and stimulates osteoclast apoptosis which can be used to study osteoporosis. N-Oleoyl-L-Serine showed high activity in an osteoblast proliferation assay.N-Oleoyl-L-Serine promotes osteoclast apoptosis by inhibiting Erk1 2 phosphorylation and expression of nuclear κB ligand (RANKL) receptor activator in bone marrow stromal cells and osteoblasts, which attenuates osteoclast populations.

CREBtide is a synthetic substrate for PKA (Km=3.9 µM), which is based on the phosphorylation sequence in d-CREB (cAMP response element binding protein).

TAT-GluR23A Fusion Peptide is a bioactive peptide comprising the GluR23A sequence—residues 869 to 877 of GluR23Y with alanine replacing tyrosine—and an 11 amino acid cell-permeable HIV Trans-Activator of Transcription (TAT) protein transduction domain (PTD). It serves as an inactive control counterpart to the glutamate receptor endocytosis inhibitor GluR23Y, devoid of crucial phosphorylation sites.

(Sar1,Ile4,8)-Angiotensin II is a functionally selective agonist for the angiotensin II type 1 receptor (AT1R), enhancing insulin-stimulated signaling of the insulin receptor (IR) and glycogen synthesis. It boosts the insulin-induced phosphorylation of Akt and GSK3α/β [1].

CD31, also known as platelet endothelial cell adhesion molecule-1 (PECAM-1), is a receptor on endothelial cells for clostridium perfringens beta-Toxin (CPB). It also functions as an ER-MP12 antigen and connects mechanical stress, metabolism, and inflammation. The CD31 peptide promotes phosphorylation of CD31 ITIM 686 and SHP2, thereby inhibiting TCR-induced T-cell activation [1]-[5].

The hepatitis B virus (HBV) core protein has been found in the nucleus, the cytoplasm, or both of HBV-infected hepatocytes. nuclear localization of the HBV core protein is negatively regulated by phosphorylation during the cell cycle.

PKCε (85-92) is a biologically active peptide that functions as a specific activator of ε-PKC and induces MARCKS phosphorylation in wild-type cells, but does not affect MARCKS phosphorylation in cells derived from knockout mice.

S3 Fragment is a biologically active peptide featuring the amino-terminal phosphorylation site unique to Xenopus ADF/cofilin, which is the target of LIM kinase (LIMK) phosphorylation. LIMK1, a pivotal regulator of the actin cytoskeleton, phosphorylates ADF/cofilin at serine-3, leading to its inactivation. As a segment of the S3 peptide harboring the serine-3 sequence, this fragment serves as a widely recognized competitive inhibitor of LIMK1.

Myristoylated AC3-I is a biologically active peptide and a myristoylated variant of the Autocamtide-3-Derived Inhibitory Peptide (AC3-I). It acts as a highly specific inhibitor of Calmodulin-Dependent Protein Kinase II (CaMKII) with enhanced resistance to proteolysis. This compound is a derivative of Autocamtide-3, where the Thr-9 phosphorylation site is replaced by Ala.

Azurin p28 peptide, a tumor-penetrating antitumor agent, stabilizes p53 by reducing its proteasomal degradation via the formation of a p28:p53 complex. It elicits apoptosis or cell cycle arrest and suppresses the growth of p53-positive tumors. Additionally, the peptide exhibits antiangiogenic properties by inhibiting the phosphorylation of VEGFR-2, FAK, and Akt [1] [2] [3].

N-myristoyl-RKRTLRRL is a compound that impedes the binding of protein kinase C (PKC) substrates and inhibits calcium (Ca2+)- and phosphatidylserine (PS)-dependent phosphorylation of histones, exhibiting an IC50 of 5 μM. Additionally, it demonstrates an inhibitory effect on histone phosphorylation with an IC50 of 80 μM [1] [2].

Malantide TFA, a synthetic dodecapeptide, originates from the phosphorylation site targeted by cAMP-dependent protein kinase (PKA) on the β-subunit of phosphorylase kinase. Exhibiting a high specificity for PKA with a Michaelis constant (Km) of 15 μM, this compound demonstrates more than 90% inhibition of substrate phosphorylation in the presence of protein inhibitor (PKI) across various rat tissue extracts [1]. Moreover, Malantide TFA acts as an effective substrate for Protein Kinase C (PKC) with a Km of 16 μM [2].

[Glycogen Synthase (1-12) Ala9,10, Lys11,12] is a selective substrate for protein kinase C (PKC) phosphorylation. It serves to assess PKC activity [1].

Cyclo(L-Phe-L-Val) is a metabolite of the sponge bacterium Pseudoalteromonas sp. NJ6-3-1 that can autoinduce production of antibacterial substances active against S. aureus when co-cultured at a low cell density. It induces neurite outgrowth and branching of chick cortical neurons in vitro when used at concentrations of 16 and 32 μM. It increases phosphorylation of the PI3K substrate Akt, and neurite outgrowth induced by cyclo(L-Phe-L-Val) can be blocked by the PI3K inhibitor LY294002 . Cyclo(L-Phe-L-Val) enhances axon sprouting of calcitonin gene-related protein positive (CGRP+) primary afferents in the spinal cord following crush injury and of serotonin neurons in uninjured spinal cord. Cyclo(L-Phe-L-Val) is also a bitter taste component of cocoa and roasted coffee.

AY 254 is a potent PAR2 biased agonist. Selectively activates ERK1/2 signaling (EC50= 2 nM for ERK1/2 phosphorylation versus 80 nM for Ca2+release). Reduces cytoKi ne-induced caspase 3/8 activation, promotes scratch-wound healing, and induces IL-8 secretion, in human colorectal cancer (HT29) cellsin vitro.

STE-MEK1(13), a cell-permeable ERK1/2 inhibitor with IC50 values ranging from 13 to 30 μM, impedes the phosphorylation of ERK1/2, as demonstrated in studies [1] [2].

S1H, a synthetic peptide mimetic of human growth hormone amino acids 36-51, acts as an antagonist to the growth hormone receptor. It forms an α-helical structure in solution and inhibits STAT5 phosphorylation triggered by human growth hormone in SK-MEL-28 and MALME-3M melanoma cell lines, as well as prolactin in IM-9 B cell lymphocytes, at concentrations of 100 and 200 nM.

Glucagon is a peptide hormone, produced by pancreatic α-cells. Glucagon reduces the activity of HNF-4. Glucagon stimulates gluconeogenesis. Glucagon enhances HNF4α phosphorylation.

[pThr3]-CDK5 Substrate TFA, a potent Phospho-Thr3CDK5 Substrate, originates from the histone H1 peptide sequence that binds to CDK5's active site. This substrate undergoes phosphorylation by CDK5, demonstrating a K_m value of 6 µM [1].

Woodtide, a substrate for the DYRK (DYRK) family of kinases, is designed based on the sequence surrounding the DYRK phosphorylation site in FKHR [1] [2].

Prolylserine, a dipeptide, acts as a melanogenesis inhibitor in Mel-Ab cells by reducing microphthalmia-associated transcription factor (MITF) and tyrosinase expression, inducing phosphorylation of ERK, but not affecting cAMP response element-binding protein (CREB) [1].

AKTide-2T TFA, serving as an optimal in vitro substrate for AKT, demonstrates competitive inhibition of histone H2B phosphorylation with a Ki value of 12 nM. It effectively mimics the optimal phosphorylation sequence of Akt and acts as an inhibitory peptide, distinct from the wildtype AKTide due to the absence of Thr at the S22 position [1].

TAT-DEF-Elk-1 TFA is a cell-penetrating peptide Elk-1 inhibitor, mimics and specifically interferes with the DEF domain of Elk-1. TAT-DEF-Elk-1 blocks Elk-1 phosphorylation and prevents Elk-1 nuclear translocation without interfering with ERK nor MSK1 act