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| 1. |
Binkowski, B., Fan, F., Wood, K.
(2009)
Engineered luciferases for molecular sensing in living cells
Curr. Opin. Biotechnol
20
,
14-8
.
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Notes:
Sophisticated tools are required to gain insight into the complicated mileau that makes up intracellular machinery. One means of gaining this insight is creation of intracellular biosensors using structurally engineered reporter proteins as biosensors. These biosensors can serve as probes within living cells, transmitting a signal regulated by the sensor is regulated by its interaction with cellular components. This article highlights the strategies behind a number of designs that have been described for preparing luciferase-containing intramolecular sensors.
(0004009) |
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Products: pCBG99-Control Vector | pCBR-Control Vector |
| 2. |
Tang, Y., Scheef, E.A., Wang, S., Sorenson, C.M., Marcus, C.B., Jefcoate, C.R. and Sheibani, N.
(2009)
CYP1B1 expression promotes the proangiogenic phenotype of endothelium through decreased intracellular oxidative stress and thrombospondin-2 expression.
Blood
113
,
744–754
.
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Notes:
The authors tested if CYP1B1 removed cellular oxygenation products that induce oxidative stress and promote the release of antiangiogenic factors. The P450-Glo™ CYP1B1 Assay was used to determine CYP1B1 activity. The presence of glutathione was assessed using either 104 retinal endothelial cells or 50µl of mouse retinal extracts dispensed into each well of a 96-well plate with the GSH-Glo™ Glutathione Assay.
(0004010) |
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Products: GSH-Glo™ Glutathione Assay | P450-Glo™ CYP1B1 Assay |
| 3. |
Brunzell, D.H., Mineur, Y.S, Neve, R.L. and Picciotto, M.R.
(2009)
Nucleus accumbens CREB activity is necessary for nicotine conditioned place preference.
Neuropsychopharmacology
Feb. 11
,
(epub ahead of print)
.
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Notes:
The authors of this study used the HRE-CRE-luciferase reporter cell line (Glo-Response™ Cells) to test HSV constructs for activity. Cells were infected with HSV-CREB, HSV-mCREB (dominant negative) or HSV-LacZ control vector. Comparisons indicated that cells transfected with HSV-CREB showed increase in CRE-mediated activity, while those transfected with HSV-mCREB showed attenuation of CRE-mediated cellular activity.
(0003956) |
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Products: GloResponse™ CRE-luc2P HEK293 Cell Line |
| 4. |
Cho, Y.Y., Tang, F., Yao, K., Lu, C., Zhu, F., Zheng, D., Pugliese, A., Bode, A.M. and Dong, Z.
(2009)
Cyclin-dependent kinase-3-mediated c-Jun phosphorylation at Ser63 and Ser73 enhances cell transformation.
Cancer Res.
69
,
272–281
.
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Notes:
This paper examined the role of the Cdk3/c-Jun signaling in EGF-stimulated cell proliferation and cell transformation. An AP-1 luciferase reporter plasmid construct was contransfected with various expression vector combinations of Cdk3, Cdk2, c-Jun, c-Jun M63/73, Cdk3-DN and cyclin C and the phRL-SV40 Vector as a normalization control. Cells were lysed at room temperature for 30 minutes with gentle shaking and luciferase activity measured using the Dual-Luciferase® Reporter Assay System. SaoS-2 cells transfected with a mock and Cdk3 RNAi vector were seeded at a density of 4 x 103 in 96-well plates with 20µl of medium. After 24 hours, 20µl of CellTiter® 96 AQueous One Solution was dispensed to each well, and the plate incubated for 1 hour at 37°C. The reaction was stopped using 25µl of 10% SDS and absorbance was measured at 492 and 690nm. For the CheckMate™ Mammalian Two-Hybrid System, the plasmid constructs, pACT-c-Jun, pBIND-Cdk3 and pG5luc, were cotransfected into HEK293 cells at no more than 100ng/well in a 48-well plate. After incubation and lysis, 20µl of lysate was dispensed into each well of a 96-well luminescence plate. Firefly and Renilla luciferase activity was detected.
(0004028) |
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Products: CellTiter 96® AQueous One Solution Cell Proliferation Assay | CheckMate™ Mammalian Two-Hybrid System | Dual-Luciferase® Reporter 1000 Assay System | Dual-Luciferase® Reporter Assay System | Dual-Luciferase® Reporter Assay System 10-Pack | pACT Vector | pBIND Vector | pG5luc Vector |
| 5. |
Staniszewska, I., Sariyer, I.K., Lecht, S., Brown, M.C., Walsh, E.M., Tuszynski, G.P., Safak, M., Lazarovici, P. and Marcinkiewicz, C.
(2008)
Integrin alpha9 beta1 is a receptor for nerve growth factor and other neurotrophins.
J. Cell Sci.
121
,
504–13
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Notes:
The authors investigated the ability of α9β1 integrin to act as a neurotrophin receptor and affect cell signaling pathways. As part of the study, RT-PCR was used to detect the presence of other neurotrophin receptors in their model cell line, SW480. Reverse transcription was performed using the Reverse Transcription System and 1µg of total RNA isolated using the SV Total RNA Isolation System. The resulting cDNA (5µg) was amplified for 35 cycles (β-actin as a control) or 40 cycles (TrkA and p75NTR). RT-PCR results were confirmed by Western blot analysis.
(0003884) |
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Products: GoTaq® Green Master Mix | Reverse Transcription System | SV Total RNA Isolation System |
| 6. |
Wong, D.J., Nuyten, D.S.A., Regev, A., Lin, M., Adler, A.S., Segal, E., van de Vijver, M.J. and Chang, H.J.
(2008)
Revealing targeted therapy for human cancer by gene module maps
Cancer Res.
68
,
369-378
.
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Notes:
The authors of this study used the gene module map method to identify genotype-specific therapies for human cancers. They studied breast cancer cell lines that expressed the "mitochondria" and "wound signatures". These cell lines, which are associated with tumors that have poor prognosis, were also shown to have a "proteasome signature" and were sensitive to the proteasome inhibitor bortezomib. The authors used the Proteasome-Glo™ Chymotrypsin-Like Cell-Based Assay to show that genotype-specific killing of "wound signature" cells was not due to differential degrees of proteasome inhibition, since 1 and 1µmol/L of bortezomib completely inhibited the ability of the wound signature and control cells to cleave the luminogenic substrate. More likely, the wound signature genotype conferred increased susceptibility to death from proteasome inhibition.
(0003870) |
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Products: Proteasome-Glo™ Chymotrypsin-Like Cell-Based Assay |
| 7. |
Joo, J.H. and Jetten, A.M.
(2008)
NF-κB-dependent transcriptional activation in lung carcinoma cells by farensol involves p65/RelA(Ser276) phosphorylation via the MEK-MSK1 signaling pathway
J. Biol. Chem.
283
,
16391-16399
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Notes:
This article showed that expression of several immune response genes could be induced in lung adenocarcinoma H460 cells by treatment with farnesol and that this induction proceeds through an NF-κB pathway. To determine which MAPKs were involved in the activation of these genes, the authors used the MEK inhibitor U0126 and showed that it inhibited the expression of several of the immune response genes and specifically inhibited the phosphorylation of p65 on Ser276.
(0003904) |
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Products: MEK Inhibitor U0126 |
| 8. |
Kannan, S., Audet, A., Huang, H., Chen, L-J. and Wu, M.
(2008)
Cholesterol-rich membrane rafts and Lyn are involved in phagocytosis during Pseudomonas aeruginosa infection
J. Immunology
180
,
2396-2408
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Notes:
The authors of this study investigated the role of Lyn, a Src-family tyrosine kinase, in regulating the formation of the phagosome in alveolar macrophages in response to Psuedomonas aeruginosa (PA) infection. The Kinase-Glo® Assay was used to assess Lyn activity, using acid-denatured enolase as the substrate. The authors found that Lyn kinase activity was increased following infection with PA.
(0003929) |
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Products: Kinase-Glo® Luminescent Kinase Assay |
| 9. |
Schröter, T., Minond, D., Weiser, A., Dao, C., Habel, J., Spicer, T., Chase, P., Baillargeon, P., Scampavia, L., Schürer, S., Chung, C., Mader, C., Southern, M., Tsinoremas, N., Lograsso, P. and Hodder, P.
(2008)
Comparison of minaturized time-resolved fluorescence resonance energy transfer and enzyme-coupled luciferase high-throughput screening assays to discover inhibitors of Rho-Kinase II (ROCK-II).
J. Biomol. Screen.
13
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17-28
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Notes:
The authors of this paper compared time-resolved, fluorescence energy transfer and ATP-based luminescent assays in ultrahigh-throughput screens (1536-well) for Rho-associated kinase II inhibitors. They found that both technologies are suitable for such a screen and perform similarly; however, they note that the ATP-based luminescent kinase assay provides an economical advantage.
(0003932) |
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Products: Kinase-Glo® Luminescent Kinase Assay |
| 10. |
Wierenga, K.J., Lai, K., Buchwald, P. and Tang, M.
(2008)
High-throughput screening for human galactokinase inhibitors.
J. Biomol. Screen.
13
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415-423
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Notes:
Thees authors searched for small-molecule inhibitors of galactokinase (GALK). They developed an HTS assay using the Kinase-Glo® Assay System. The HTS assay used 15 μM ATP and α-D-galactose as the substrate and was performed in 384-well plates against 50,000 small molecules. Two hundred compounds were identified from the primary screen as GALK inhibitors.
(0003934) |
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Products: Kinase-Glo® Luminescent Kinase Assay |
| 11. |
Tatematsu, K., Yoshimoto, N., Okajima, T., Tanizawa, K., and Kuroda, S.
(2008)
Identification of ubiquitin ligase activity of RBCK1 and its inhibition by splice variant RBCK2 and protein kinase Cβ.
J. Biol. Chem.
283
,
11575-11585
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Notes:
RBCK1 is a RING-IBR (ring in between ring fingers) protein previously shown to have transcriptional activity and to bind protein Kinase Cβ. This paper demonstrates that RBCK1 also posseses ubiquitin ligase E3 activity. Both FLAG-tag and HaloTag® labeled proteins were used to demonstrate this activity. To demonstrate the interaction between RBCK1 and ubiquitinated proteins, HaloTag®-ubiquitin and FLAG-RBCK1 were coexpressed in HEK293 cells in the presence or absence of a proteasome inhibitor. The anti-FLAG immunoprecipitates isolated from these cells were analyzed by SDS-PAGE and Western blotting using anti-HaloTag® and anti-FLAG antibodies and self-ubiquitination of RBCK1 was demonstrated. RBCK2, a splice variant of RBCK1 lacking the RING domain showed no self ubiquitination activity but was demonstrated to interact with RBCK1 in vivo and in vitro, and to inhibit the self-ubiquitination activity of RBCK1 in a FLAG-tag assay. Pulse-chase experiments, using HEK293 cells expressing HaloTag®-RBCK1 with or without RBCK2 and treated with HaloTag®-TMR ligand, were used to show that the half-life of RBCK1 was extended by overexpression of RBCK2.
(0003874) |
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Products: Anti-HaloTag® pAb | HaloTag® pHT2 Vector | HaloTag® TMR Ligand |
| 12. |
Ogawa, M., Shinohara, H., Sakagami, Y. and Matsubayashi, Y.
(2008)
Arabidopsis CLV3 peptide directly binds CLV1 ectodomain.
Science
319
,
294
.
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Notes:
The authors of this study investigated the role of the genes CLV1 and CLV3 stem cell renewal and differentiation in self-renewing shoot apical meristem (SAM) in Arabidopsis. CLV1 encodes a receptor kinase that is a negative regulator of cell growth, and therefore cannot be overexpressed in plant cells. CLV3, which encodes a protein that is processed to a 12-amino acid peptide, is believed to be a ligand for CLV1. In this study, the authors made a construct in which the CLV1 kinase domain was replaced with the HaloTag™ protein and expressed the fusion protein in tobacco BY-2 cells. The fusion protein was detected using the HaloTag™ TMR ligand. They next incubated membrane extracts from wildtype and transgenic BY-2 cells (expressing the HaloTag™-CLV1 fusion) with tritium-labeled CLV3. The transgenic cells showed significantly higher CLV3 binding than wildtype, and the authors show that CLV3 specifically labels a 130-kd band that corresponds to the HaloTag™-CLV1 fusion protein, indicating that CLV3 binds the ectodomain of CLV1.
(0003763) |
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Products: HaloTag® pHT2 Vector | HaloTag® TMR Ligand |
| 13. |
Hahn, C.K., Ross, K.N., Warrington, I.M., Mazitschek, R., Kanegai, C.M., Wright, R.D., Kung, A.L., Golub, T.R. and Stegmaier, K.
(2008)
Expression-based screening identifies the combination of histone deacetylase inhibitors and retinoids for neuroblastoma differentiation.
Proc. Natl. Acad. Sci. USA
105
,
9751-9756
.
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Notes:
The authors designed a high-throughput gene-expression screen to identify compounds that induce a neuroblastoma gene signature in BE(2)-C cells. The screen used Valproic Acid (VPA), an inhibitor of histone deacetylase, as an enhancer. The top hit from the screen was all-trans retinoic acid (ATRA). The authors proposed that ATRA + VPA would reduce cell viability and might induce apoptosis by inducing genes associated with terminal differentiation. They used the CellTiter-Glo® Luminescent Cell Viability Assay in a 96-well format to assess the effects of ATRA and a variety of inhibitors of histone deacetylase on BE(2)-C cell viability.
(0003931) |
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Products: CellTiter-Glo® Luminescent Cell Viability Assay |
| 14. |
Lin, H., Lee, E., Hestir, K., Leo, C., Huang, M., Bosch, E., Halenbeck, R., Wu, G., Zhou, A., Behrens, D., Hollenboguh, D., Linnemann, T., Qin, M., Wong, J., Chu, K., Doberstein, S.K. and Williams, L.T.
(2008)
Discovery of a cytokine and its receptor by functional screening of the extracellular proteome.
Science
320
,
807-11
.
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Notes:
The authors of this study created a cDNA library representative of the extracellular proteome (secreted proteins and the extracellular domains of transmembrane proteins). Each cDNA was individually transfected into 293T cells. Medium from the cDNA of each transfection was used in a suite of cell-based assays. The CellTiter-Glo® Assay was used to screen for secreted factors from the cell lines expressing the cDNA that affected viability of twelve cell lines: human primary B cells, human primary T cells, human primary NK cells, human primary monocytes, A549 cells, Colo205 cells, U-118 cells, MDA-MB231 cells, PC3 cells, PANC1 cells, human primary skeletal muscle progenitor cells, and rat primary oligodendrocyte precursor cells.
(0003935) |
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Products: CellTiter-Glo® Luminescent Cell Viability Assay |
| 15. |
Case, M., Matheson, E., Minto, L., Hassan, R., Harrison, C.J., Bown, N., Bailey, S., Vormoor, J., Hall, A.G. and Irving, J.A.E.
(2008)
Mutation of genes affecting the RAS pathway is common in childhood acute lymphoblastic leukemia
Cancer Res.
68
,
6803-6809
.
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Notes:
The authors of this study investigated the relationship of somatic mutations that deregulate the RAS-RAF-MEK-ERK pathway and Acute Lymphoblastic Leukemia (ALL) and its progression to relapse in some patients. They show that such mutations are common in ALL and its recurrence. Furthermore, lymphoblasts from patients with mutations that were associated with upregulation of ERK showed increased cytotoxicity over wild-type controls when treated with U0126, suggesting that specific ERK inhibitors may eventually yield useful therapeutics. Following drug exposure, cytotoxic effects were assessed using the CellTiter 96® AQueous One Solution Cell Proliferation Assay.
(0003905) |
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Products: CellTiter 96® AQueous One Solution Cell Proliferation Assay | MEK Inhibitor U0126 |
| 16. |
Seyb, K.I., Schuman, E.R., Ni, J., Huang, M.M., Michaelis, M.L., and Glicksman, M.A.
(2008)
Identification of small molecule inhibitors of β-amyloid cytotoxicity through a cell-based high-throughput sreening platform.
J. Biomol. Screening
13
,
870-878
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Notes:
This paper demonstrates use of a calpain assay in a cell-based format. (Calpain-Glo™ Assay).
(0003941) |
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Products: Calpain-Glo™ Protease Assay |
| 17. |
Kawaguchi, T., Chen, Y.P., Norman, R.S. and Deecho, A.W.
(2008)
Rapid screening of quorum-sensing signal N-acyl homoserine lactones by an in vitro cell-free assay.
Appl. Environ. Microbiol.
74
,
3667-3671
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Notes:
The authors of this paper describe the development of a cell-free assay system derived from Agrobacterium tumefaciens NTL4(pCF218) (pCF372), which expresses β-galactosidase under the control of a tra1 promoter. The tra1 promoter is responsive to quorum-sensing signals. The assay was developed to address time-consuming cell conditioning and incubation times of the standard whole-cell assays used to detect quorum-sensing signals in natural systems. Replacing the X-Gal substrate with the luminescent Beta-Glo® substrate increased the assay sensitivity by tenfold.
(0003936) |
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Products: Beta-Glo® Assay System |
| 18. |
Simonetti, M., Giniatullin, R., and Fabbretti, E.
(2008)
Mechanism mediating the enhanced transcription of P2X3 receptor gene by calcitonin gene related peptide in trigeminal sensory neurons.
J. Biol. Chem.
May 6
,
Epub (ahead of print)
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Notes:
These authors investigated the mechanism of action of the migraine mediator calcitonin gene-related peptide (CGRP), which is known to sensitize the P2X3 pain receptors to increase impulse flow to brain stem trigeminal nuclei. They showed that CAM KII inhibitors prevented CGRP-induced upregulation of P2X3 mRNA using real-time RT-PCR, and then confirmed that active CAM KII was involved in the signaling mechanism by staining with Anti-ACTIVE® CAM KII Antibodies. The immunoreactivity was upregulated by CGRP treatment of trigeminal neurons, and the distribution of the active CAM KII was localized to the membrane region. They then examined the mechanism of transcriptional activation of the P2X3 pain receptor genes and showed that the transcription factor CREB, which is known to be dependent on CAM KII for activation and nuclear localization, was involved. The authors also investigated the role of BDNF in the process, because CGRP is known to promote BDNF expression by trigeminal neurons, and because BDNF is thought to be involved in pain processing. They used the BDNF Emax Immunoassay System to measure BDNF levels in culture media after application of CGRP to neuronal cell cultures, and demonstrated that there was a fourfold increase in BDNF after CGRP exposure. They also showed that BDNF promoted CAMKII and CREB activation.
(0003873) |
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Products: Anti-ACTIVE® CaM KII pAb, Rabbit, (pT286) | BDNF Emax® ImmunoAssay System |
| 19. |
Chang, Q,. Bhatia, D., Zhang, Y., Meighan, T., Castranova, V., Shi, X. and Chen, F.
(2008)
Incorporation of an internal ribosome entry site-dependent mechanism in arsenic-induced GADD45 alpha expression.
Cancer Res.
2007
,
6146–54
.
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Notes:
Trivalent arsenic (As3+) induces expression of growth arrest- and DNA damage-induced gene 45α (GADD45α), which interacts with intracellular signaling molecules involved in cell cycle regulation, apoptosis and immune response. To characterize GADD45α mRNA expression patterns, total RNA was isolated from untreated (growing) and As3+-treated (arrested) BEAS-2B cells, and GADD45α mRNA was amplified using the AccessQuick™ RT-PCR System. GADD45α mRNA levels were undetectable in growing cells but increased in a time-dependent manner in arrested cells. Reverse transcription was carried out at 45°C for 50 minutes, followed by 35 cycles of PCR.
(0003766) |
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Products: AccessQuick™ RT-PCR System |
| 20. |
Rubin, E., Wu, X., Zhu, T., Cheung, J.C., Chen, H., Lorincz, A., Pandita, R.K., Sharma, G.G., Ha, H.C., Gasson, J., Hanakahi, L.A., Pandita, T.K. and Sukumar, S.
(2007)
A role for the HOXB7 homeodomain protein in DNA repair.
Cancer Res.
67
,
1527–35
.
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Notes:
These authors searched for proteins that interact with HOXB7 to help confirm resistance to ionizing radiation in human mammary epithelial cells. They identify four HOXB7-binding proteins as members of the DNA-dependent protein kinase (DNA-PK) holoenzyme. DNA-PK assays were performed according to the manufacturer's instructions. HOXB7 was shown to stimulate DNA-PK activity.
(0003611) |
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Products: SignaTECT® DNA-Dependent Protein Kinase Assay System |
| 21. |
Huang, L., Ho, P. and Chen, C-H.
(2007)
Activation and inhibition of the proteasome by betulinic acid and its derivatives
FEBS Lett.
581
,
4955-4959
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Notes:
The authors of this study investigated the effects of betulinic acid (BA) and its chemical derivatives on the proteasome in vitro and in cells. They used the Proteasome-Glo™ Chymotrypsin-Like Cell-Based Assay to assess the effects of BA derivatives on proteasome activity in MT4 cells.
(0003871) |
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Products: Proteasome-Glo™ Chymotrypsin-Like Cell-Based Assay |
| 22. |
Andreozzi, F., Laratta, E., Procopio, C., Hribal, M.L., Sciacqua, A., Perticone, M., Miele, C., Perticone, F., and Sesti, G.
(2007)
Interleukin-6 impairs the insulin signaling pathway, promoting production of nitric oxide in human umbilical vein endothelial cells.
Mol. Cell. Biol.
27
,
2372-2383
.
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Notes:
The authors used the ProFluor™ Ser/Thr PPase Assay to assess the effect of several hormones and inhibitors on Protein Phosphatase 1 (PP1) activity in human umbilical vein endothelial cells. Specifically they tested whether insulin increased PP1 activity in HUVECs, as has been shown in cardiomyocytes, and whether this activity was affected by IL-6.
(0003593) |
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Products: ProFluor® Ser/Thr PPase Assay |
| 23. |
Zhang, Y-w., Wang, R., Liu, Q., Zhang, H., Liao, F-F. and Xu, H.
(2007)
Presenilin/γ-secretase-dependent processing of β-amyloid precursor protein regulates EGF receptor expression
Proc. Natl. Acad. Sci. U S A
104
,
10613-10618
.
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Notes:
The authors of this study investigated the downstream effects of the release of the intracellular domain of the Amyloid-β precursor protein (AICD) on cellular activities. They amplified the 5′ region of the mouse EGFR gene and cloned it into a pGL3 vector. This construct was cotransfected into embryonic fibroblasts derived from APP/APLP2 DKO mice along with a vector expressing AICD, AICD and the multidomain protein Fe65, Fe65 alone or NotchΔE, along with a Renilla control vector to normalize data for transfection efficiency. The data indicate that AICD negatively regulates transcription of the EGF Receptor gene.
(0003861) |
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Products: pGL3-Promoter Vector | pRL-SV40 Vector |
| 24. |
Davis, R. E., Zhang, Y-Q., Suthall, N., Staudt, L.M., Austin, C.P., Inglese, J. and Auld, D.S.
(2007)
A cell-based assay for IκBα stabilization using a two-color dual luciferase-based sensor
ASSAY and Drug Development Technologies
5
,
85-103
.
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Notes:
The Chroma-Luc™ vectors, which encode red light-emitting and green-light emitting beetle luciferases, were used to develop an HTS cell-sensor assay (1536-well format) to detect IκBα stabilization. The assay was able to identify specific stabilizers of IκBα. Known and novel inhibitors of NFκB signaling were detected in the assay.
(0003727) |
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Products: Chroma-Glo™ Luciferase Assay System | pCBG68-Basic Vector | pCBG68-Control Vector | pCBG99-Basic Vector | pCBG99-Control Vector | pCBR-Basic Vector | pCBR-Control Vector |
| 25. |
Maekawa, M., Yamamoto, T., Kohno, M., Takeichi, M. and Nishida, E.
(2007)
Requirement for ERK MAP kinase in mouse preimplantation development
Development
134
,
2751-2759
.
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Notes:
The authors of this study investigated the role of ERK1/2 kinase signaling in the preimplantation developmental events that precede compaction and blastocyst formation (2-cell to 8-cell stages). The MEK inhibitor U0126 was added to 2-cell stage mouse embryos, and the embryos were observed to arrest at the 4-cell stage. The arrest was reversible, but experiments indicated that ERK1/2 signaling is required for M-phase progression in early cell cycles during mouse development.
(0003906) |
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Products: MEK Inhibitor U0126 |