dephosphorylation

NFAT Inhibitor (VIVIT peptide) 是NFAT 的细胞渗透性肽抑制剂，能够选择性抑制钙调磷酸酶介导的NFAT 脱磷酸作用。

MT 63-78 是一种有效的直接AMPK 激活剂，EC50为 25 μM。它诱导细胞有丝分裂阻滞和细胞凋亡，通过抑制脂肪生成和mTORC1途径来阻止前列腺癌的生长，具有抗肿瘤作用。

EB-3D 是一种选择性胆碱激酶 α 抑制剂，对 ChoKα1 的IC50值为 1 μM。它影响 ChoKα 表达、AMPK 激活、细胞凋亡、内质网应激和脂质代谢，具有抗癌活性。

DD1 (HUN85111) 是一种蛋白酶体抑制剂，可诱导人髓系肿瘤选择性凋亡。

Cyt-PTPε Inhibitor-1 (A Inhibitor-1) 是胞质蛋白酪氨酸磷酸酶 ε 的抑制剂。 Cyt-PTPε Inhibitor-1 阻断 c-Src 的去磷酸化并表现出抗破骨活性。

Adenosine 5'-diphosphate (ADP) 属于天然核苷酸，由 ATP 去磷酸化得到。Adenosine 5'-diphosphate 对细胞代谢至关重要，还可诱导血小板聚集。

L-Ascorbic acid 2-phosphate trisodium (Sodium ascorbyl phosphate) 是长效的维生素 C 衍生物，能够刺激胶原蛋白的表达和形成。Sodium L-ascorbyl-2-phosphate 提高成骨细胞分化过程中 hASC 中的碱性磷酸酶活性和 runx2A 的表达，因此，能够促进人脂肪干细胞的成骨分化。

Lenaldekar (LDK) 抑制 T 细胞扩增和自身免疫性脑脊髓炎。 Lenaldekar 导致 PI3 激酶 AKT mTOR 通路成员的去磷酸化并延迟有丝分裂晚期的敏感细胞。

MLi-2 是一种结构新颖、高效、选择性的 LRRK2 激酶抑制剂，具有中枢神经系统活性，IC50为 0.76 nM，有潜力用于帕金森氏病。

DDO-3733 是 ProteinPhosphatase5 (PP5) 的一种非 TRP 依赖性变构激活剂，能够有效促进下游底物的脱磷酸化。

Bacitracin Zinc 是 C55-异戊二烯焦磷酸酯的去磷酸化干扰物，可抑制 Met-enkephalin 中 Tyr 的裂解，IC50为10 μM。

A-83586C is a depsipeptide antibiotic from Streptomyces karnatakensis with potent against Gram-positive activity in vitro. A-83586C acts as a highly potent inhibitor of beta-catenin/TCF4 signaling within cancer cells, while simultaneously downregulating o

MPT0B206 is a novel tubulin polymerization inhibitor. MPT0B206 induced G2/M cell cycle arrest and the appearance of the mitotic marker MPM-2 in K562 and K562R cells, which is associated with the upregulation of cyclin B1 and the dephosphorylation of Cdc2.

N-Stearoylsphingosine (Cer(d18:1 18:0)) 是一种广泛存在真核生物体内的酰胺类化合物，通过干扰PP2A与PP2A抑制剂2的结合来增强蛋白质磷酸酶2A(PP2A)活性，导致Akt去磷酸化。N-Stearoylsphingosine 可用于研究前列腺癌。

Q134R, a neuroprotective hydroxyquinoline derivative that suppresses nuclear factor of activated T cell (NFAT) signaling. Q134R can across blood-brain barrier. Q134R has the potential for Alzheimer’s disease (AD) and aging-related disorders research[1]. Q134R (1-10 μM) suppresses NFAT signaling, without inhibiting calcineurin activity. Q134R partially inhibits NFAT activity in primary rat astrocytes, but does not prevent calcineurin-mediated dephosphorylation of a non-NFAT target, either in vivo, or in vitro[1]. Q134R (4 mg kg; orally gavage; twice per day; for 7 days) treatment improves cognitive function in rodent models of AD‐like pathology[1]. [1]. Pradoldej Sompol, et al. Q134R: Small chemical compound with NFAT inhibitory properties improves behavioral performance and synapse function in mouse models of amyloid pathology. Aging Cell. 2021 Jul;20(7):e13416.

The inositol phosphates are a family of mono- to poly-phosphorylated compounds that act as messengers, regulating cellular functions including cell cycling, apoptosis, differentiation, andmotility. D-myo-Inositol-1,5,6-triphosphate is an intermediate compound, produced by the dephosphorylation of various inositol-tetrakisphosphate forms. The triphosphate can be further metabolized to produce inositol-biphosphate mediators. The biological roles of D-myo-inositol-1,5,6-triphosphate remain to be determined.

D-myo-Inositol-4-phosphate (Ins(4)P1) is a member of the inositol phosphate (InsP) molecular family that play critical roles as small, soluble second messengers in the transmission of cellular signals. The most studied InsP, Ins(1,4,5)P3, is a second messenger produced in cells by phospholipase C (PLC)-mediated hydrolysis of phosphatidylinositol-4,5-diphosphate. Binding of Ins(1,4,5)P3 to its receptor on the endoplasmic reticulum results in opening of the calcium channels and an increase in intracellular calcium. Ins(4)P1 can be formed by dephosphorylation of Ins(1,4)P2 by inositol polyphosphate 1-phosphatase or dephosphorylated to inositol by inositol monophosphatase.

DiIC1(5) is a signal-off fluorescent probe for the detection of mitochondrial membrane potential disruption. It accumulates in mitochondria and its fluorescence intensity decreases when the mitochondrial membrane potential is disrupted. DilC1(5) has been used in combination with a variety of cell damage and cell death markers to classify nine stages of cell death using flow cytometry. It has also been used as a quencher for the detection of serine phosphorylation and tyrosine dephosphorylation post-translational modifications (PTMs) in quenching resonance energy transfer (QRET) and mTR-FRET applications. It displays excitation emission maxima of 659 666 nm, respectively.

Succinyladenosine is a biochemical marker of adenylosuccinase (ASL) deficiency. It is formed through the dephosphorylation of intracellular adenylosuccinic acid (S-AMP) by cytosolic 5-nucleotidase [1].

Cyclocreatine, a Creatine analogue, exhibits potent bioenergetic protection by elevating ATP levels. It demonstrates the ability to traverse cell membranes, including the blood-brain barrier, wherein it undergoes phosphorylation and dephosphorylation by creatine kinases.

BTO-1 is a compound known as a Polo-like kinase (Plk) inhibitor, commonly employed for its effectiveness in regulating processes involving phosphorylation and dephosphorylation.

LG308 是一种新型合成化合物，具有抗微管活性。LG308 诱导细胞凋亡和细胞死亡，并且显著抑制肿瘤生长，具有前列腺癌的研究潜力。LG308 诱导有丝分裂阻滞并显着抑制 G2 M 的进程，这与细胞周期蛋白 B1 和有丝分裂标志物 MPM-2 的上调以及 cdc2 的去磷酸化有关。

CBP501 is a peptide with G2 checkpoint-abrogating activity. G2 checkpoint inhibitor CBP501 inhibits multiple serine threonine kinases, including MAPKAP-K2, C-Tak1, and CHK1, that phosphorylate serine 216 of the dual-specific phosphatase Cdc25C (cell division checkpoint 25 C); disruption of Cdc25C activity results in the inhibition of Cdc25C dephosphorylation of the mitotic cyclin-dependent kinase complex Cdc2 cyclin B, preventing entry into the mitotic phase of the cell cycle.

CGP74514A is a CDK1 inhibitor with potential anticancer activity. In U937 cells, CGP74514A - induced apoptosis (5 microM) became apparent within 4 hr and approached 100% by 24 hr. The pan- caspase inhibitor Boc-fmk and the caspase-8 inhibitor lETD-fmk opposed CGP74514A -induced caspase-9 activation and PARP degradation, but not cytochrome c or Smac DIABLO release. CGP74514A -mediated apoptosis was substantially blocked by ectopic expression of full-length Bel- 2, a loop-deleted mutant Bcl-2, and Bcl-x(L). CGP74514A treatment (5 microM; 18 hr) resulted in increased p21(CIP1) expression, p27(KIP1) degradation, diminished E2F1 expression, and dephosphorylation of p34(CDC2). It also induced early (i.e., within 2 hr) inhibition of CDK1 activity and dephosphorylation of pRb, followed by pRb degradation, but did not block pRb phosphorylation at CDK2- and CDK4- specific sites. These findings indicate that the selective CDK1 inhibitor, CGP74514A , induces complex changes in cell cycle......