RSK Inhibitor, SL0101, CAS 77307-50-7, is a cell-permeable, selective, reversible, ATP-competitive RSK inhibitor (IC50 = 89 nM with 10 µM ATP). Blocks the proliferation of MCF-7 cell line. - Find MSDS or SDS, a COA, data sheets and more information.
RSK Inhibitor, SL0101, CAS 77307-50-7, is a cell-permeable, selective, reversible, ATP-competitive RSK inhibitor (IC50 = 89 nM with 10 µM ATP). Blocks the proliferation of MCF-7 cell line. - Find MSDS or SDS, a COA, data sheets and more information.
Stimulation of the Ras pathway results in the activation of ERK and RSK, but the precise mechanisms involved in RSK activation and inactivation remain elusive. In this study, we characterized the ERK binding domain of RSK1 and found that a serine residue located near the docking site (position 749 in avian RSK1) was involved in the regulation of ERK1/2 binding (Fig. 1 to 3). We also found that Ser749 was efficiently phosphorylated by the RSK1 N-terminal kinase domain in vitro (Fig. 4) and that mutations in the RSK1 kinase domains disrupted ERK dissociation (Fig. 5). Analysis of different RSK isoforms revealed that RSK1 and RSK2 activation induced ERK1/2 release but that mitogen stimulation did not affect the interaction of ERK1/2 with RSK3 (Fig. 6). We also found that RSK3 remains activated longer than RSK1 and RSK2 (Fig. 7), indicating that ERK association promotes RSK activation or antagonizes RSK inactivation.. Our results indicate that the minimal region in RSK1 necessary for ERK1/2 docking ...
BI-D1870 is a potent and specific RSK inhibitor (the p90 ribosomal S6 kinase), which inhibits RSK1, RSK2, RSK3 and RSK4 in vitro with an IC50 of 10Â-30 nM. BI-D1870 exhibited a dose-responsive antiproliferative effect on OSCC cells with relative sparing of normal human oral keratinocytes. The compound inhibited the downstream RSK target YB-1 and caused apoptosis. In addition, BI-D1870 also induced G2/M arrest by modulating the expression of p21 and other cell cycle regulators. BI-D1870 may be of useful in oral squamous cell carcinoma therapy.
Phosphorylation of the C terminus of c-Fos has been implicated in serum response element-mediated repression of c-fos transcription after its induction by serum growth factors. The growth-regulated enzymes responsible for this phosphorylation in early G1 phase of the cell cycle and the sites of phosphorylation have not been identified. We now provide evidence that two growth-regulated, nucleus- and cytoplasm-localized protein kinases, 90-kDa ribosomal S6 kinase (RSK) and mitogen-activated protein kinase (MAP kinase), contribute to the serum-induced phosphorylation of c-Fos. The major phosphopeptides derived from biosynthetically labeled c-Fos correspond to phosphopeptides generated after phosphorylation of c-Fos in vitro with both RSK and MAP kinase. The phosphorylation sites identified for RSK (Ser-362) and MAP kinase (Ser-374) are in the transrepression domain. Cooperative phosphorylation at these sites by both enzymes was observed in vitro and reflected in vivo by the predominance of the ...
Our previous study demonstrated that the total p90 ribosomal S6 kinase 2 (RSK2) protein level was significantly higher in human skin cancer tissues and cancer cells compared with normal skin tissues and premalignant cell lines. We also demonstrated that the N-terminal kinase domain of RSK2 plays an important role in transducing the RSK2 activation signal to its substrates. RSK2 requires activation of its C-terminal domain by its upstream kinases, ERKs, in order to phosphorylate and activate its substrates. For example, a recombinant RSK2 protein purified from E. Coli cannot phosphorylate the RSK2 substrate, NFAT3, but phosphorylation of RSK2 by ERKs at the linker region of RSK2 gives RSK2 the ability to phosphorylate its substrates through its N-terminal kinase domain. This suggests that ERKs/RSK2 signaling plays an important role in RSK2-mediated cell proliferation and cell transformation. Importantly, our study demonstrated that co-expression of RasG12V and RSK2 in NIH3T3 cells increased foci ...
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Recombinant full-length human RSK1 was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag. RSK1 is a member of the RSK (ribosomal S6 kinase) family that consists of growth factor-regulated serine/threonine kinases.
Recombinant full-length human RSK2 was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag. RSK2 is a member of the RSK (ribosomal S6 kinase) family that are growth factor-regulated serine-threonine kinases.
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Aret-Stav s.r.o. - in en rsk s t ,zemn protlaky,stavebn pr ce, i t n kanalizace,demont parovodu,plynovodu,d lkovodu,rozvod a jejich likvidace.
article{955774, abstract = {Among the mitogen-activated protein kinase (MAPK) targets, MSKs (mitogen- and stress-activated protein kinases) comprise a particularly interesting protein family. Because MSKs can be activated by both extracellular-signal-regulated kinase and p38 MAPKs, they are activated by many physiological and pathological stimuli. About ten years after their original discovery, they have been recognized as versatile kinases regulating gene transcription at multiple levels. MSKs directly target transcription factors, such as cAMP-response-element-binding protein and nuclear factor-kappaB, thereby enhancing their transcriptional activity. They also induce histone phosphorylation, which is accompanied by chromatin relaxation and facilitated binding of additional regulatory proteins. Here, we review the current knowledge on MSK activation and its molecular targets, focusing on recent insights into the role of MSKs at multiple levels of transcriptional regulation.}, author = ...
Y-box binding protein-1 (YB-1) is the first reported oncogenic transcription factor to induce the tumor-initiating cell (TIC) surface marker CD44 in triple-negative breast cancer (TNBC) cells. In order for CD44 to be induced, YB-1 must be phosphorylated at S102 by p90 ribosomal S6 kinase (RSK). We therefore questioned whether RSK might be a tractable molecular target to eliminate TICs. In support of this idea, injection of MDA-MB-231 cells expressing Flag-YB-1 into mice increased tumor growth as well as enhanced CD44 expression. Despite enrichment for TICs, these cells were sensitive to RSK inhibition when treated ex vivo with BI-D1870. Targeting RSK2 with small interfering RNA (siRNA) or small molecule RSK kinase inhibitors (SL0101 and BI-D1870) blocked TNBC monolayer cell growth by similar to 100%. In a diverse panel of breast tumor cell line models RSK2 siRNA predominantly targeted models of TNBC. RSK2 inhibition decreased CD44 promoter activity, CD44 mRNA, protein expression, and mammosphere ...
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PAH is a high mortality disease with no medical cure resulting in increased PAP culminating in RV failure and premature death.The vasculopathy of PAH is characterized by medial hypertrophy coupled with obliterative intimal and plexiform lesions.Current therapies do not reverse the vasculopathy.There is a need to identify additional therapeutic targets.The vasculopathy of PAH is typified by increased rates of proliferation thus raising interest in identification of novel anti-proliferative therapeutic targets. Objective: To elucidate the role of MEK/ERK/RSK90 on mitogen-induced proliferation in human PASMC. Methods: PASMC were exposed to select mitogens such as ET-1, serotonin (5-HT) and PDGF for 24h and assessed for proliferative responses using the MTT assay.To assess the role of the MEK/ERK/RSK90 signaling pathway, cultures were preincubated with select MAP Kinase inhibitors including MAPK/ERK (extracellular signal-regulated kinase) kinase (MEK) inhibitor (PD98059), p90 Ribosomal S6 ...
Impact of BI-D on HIV-1 replication and production.A. SupT1 cells were infected with HIV-1 LAI and cultured in the absence or presence of BI-D (700 nM, 5x EC50)
Protein Tob1 is a protein that in humans is encoded by the TOB1 gene. This gene encodes a member of the tob/btg1 family of anti-proliferative proteins that have the potential to regulate cell growth. When exogenously expressed, this protein suppresses cell growth in tissue culture. The protein undergoes phosphorylation by a serine/threonine kinase, 90 kDa ribosomal S6 kinase. Interactions of this protein with the v-erb-b2 erythroblastic leukemia viral oncogene homolog 2 gene product p185 interferes with growth suppression. This protein inhibits T cell proliferation and transcription of cytokines and cyclins. The protein interacts with both mothers against decapentaplegic Drosophila homolog 2 and 4 to enhance their DNA binding activity. This interaction inhibits interleukin 2 transcription in T cells. TOB1 has been shown to interact with: CNOT7, MAPK1 MARCKS, Mitogen-activated protein kinase 9, and RPS6KA1. GRCh38: Ensembl release 89: ENSG00000141232 - Ensembl, May 2017 GRCm38: Ensembl release ...
Study Flashcards On MSK 12 at Cram.com. Quickly memorize the terms, phrases and much more. Cram.com makes it easy to get the grade you want!
Aret-Stav s.r.o. - in en rsk s t ,zemn protlaky,stavebn pr ce, i t n kanalizace,demont parovodu,plynovodu,d lkovodu,rozvod a jejich likvidace.
Välkommen till veterinär Elisabeth Hemberg, jag har stor erfarenhet av dräktighetsproblem hos ston. Ston mottages för inseminering med färsk eller frusen sperma.
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G-protein-coupled receptor agonists are powerful stimulators of mitogen-activated protein kinase (MAPK) cascades in cardiac myocytes. However, little is known regarding the physiological activation of enzymes downstream of MAPKs. We examined the activation of mitogen- and stress-activated protein kinase-1 (MSK1), a downstream target of MAPKs, in adult rat cardiac myocytes by phenylephrine and endothelin-1. Both agonists induced the phosphorylation of MSK1 at Thr-581 and Ser-376 but not at Ser-360. Maximal phosphorylation was observed at 10-15min after stimulation and it correlated with increased activity. Maximal activation of MSK1 in adult cardiomyocytes temporally coincided with maximal p38 MAPK activation while activation of the extracellular-signal-regulated kinase (ERK) cascade was more rapid. Phosphorylation and activation of MSK1 was completely inhibited by either PD98059 (ERK1/2 pathway inhibitor) or SB203580 (p38 MAPK inhibitor) alone. These data demonstrate that MSK1 activation in ...
TY - JOUR. T1 - A clickable inhibitor reveals context-dependent autoactivation of p90 RSK. AU - Cohen, Michael S.. AU - Hadjivassiliou, Haralambos. AU - Taunton, Jack. PY - 2007/3. Y1 - 2007/3. N2 - p90 ribosomal protein S6 kinases (RSKs) integrate upstream signals through two catalytic domains. Autophosphorylation of Ser386 by the regulatory C-terminal kinase domain (CTD) is thought to be essential for activation of the N-terminal kinase domain (NTD), which phosphorylates multiple downstream targets. We recently reported fmk, an irreversible inhibitor of the CTD of RSK1 and RSK2. Here we describe fmk-pa, a propargylamine variant that has improved cellular potency and a clickable tag for assessing the extent and selectivity of covalent RSK modification. Copper-catalyzed conjugation of an azidoalkyl reporter (the click reaction) revealed that fmk-pa achieves selective and saturable modification of endogenous RSK1 and RSK2 in mammalian cells. Saturating concentrations of fmk-pa inhibited Ser386 ...
The results presented here reveal that activation of p90RSK inhibited Ito,f, IK,slow, and ISS and led to the prolongation of cardiac repolarization without affecting mRNA levels of Kv subunits. Ito,f decrease was caused by p90RSK phosphorylating Kv4.3 subunit and reduction of IK,slowwas due to p90RSK inhibiting Kv1.5-encoded channel activity. H2O2, a mediator of induced cardiac p90RSK activation in ischemia/reperfusion injury and diabetes mellitus, had effects similar to p90RSK in the modulation of Kv4.3 or Kv4.3 and KChIP2-encoded channel activity. Importantly, a p90RSK-specific inhibitor, fmk,23 was able to abolish H2O2s effects on Kv4.3 channel activity and rescued the mouse ventricular K+ channel activity inhibited by p90RSK. To our knowledge, this is the first report to document that activation of p90RSK leads to the prolongation of cardiac repolarization by inhibiting voltage-gated outward K+ currents.. Downregulation of outward K+ currents (Ito,f) has been observed in a variety of ...
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The growth factor-regulated ribosomal S6 kinase RSK2 appears to be essential for osteoblast function, since mice lacking RSK2 are osteopenic because of a cell-autonomous defect in osteoblast activity. In contrast, osteoclast differentiation was unaffected in vivo and in vitro in the absence of RSK2. However, the development of c-Fos-induced osteosarcomas was found to be dependent on RSK2-mediated c-Fos posttranscriptional regulation. Thus, important functions of c-Fos are determined by RSK2-mediated posttranscriptional mechanisms, which may also be required in human osteosarcomas and in CLS.. Humans carrying mutations of RSK2 suffer from CLS, an X-linked mental retardation condition associated with progressive skeletal deformities and osteopenia, delayed bone age, and delayed fontanelle closure (18). It has been shown that mice lacking RSK2 also have impaired learning and cognitive functions (19). Interestingly, mice lacking c-fos in the CNS have similar learning and behavior deficits (27). ...
OxLDL drives NF-κB activation and VCAM-1 expression through integrin-α5β1-dependent FAK signaling; however, the mechanisms regulating FAK-dependent NF-κB signaling have remained elusive (Yurdagul et al., 2014). Here, we define a new signaling pathway involving FAK-dependent activation of the RSK pathway to promote NF-κB activation through its classic upstream mediator IKKβ. Although both RSK and NF-κB activation are known to be redox sensitive, we show that preventing integrin signaling or FAK activation does not significantly affect oxLDL-induced ROS levels, suggesting that FAK-dependent activation of the RSK-IKKβ-NK-κB pathway operates independently from oxidative stress (Abe et al., 2000; Kabe et al., 2005). Instead, oxLDL drives FAK-dependent ERK activation that results in RSK-dependent signaling to IKKβ and NF-κB. We further demonstrate elevated FAK activation in the endothelium overlying both mouse and human atherosclerotic plaques, and show that transgenic mice containing an ...
Although we demonstrated that pp90RSK is activated by GM-CSF and able to phosphorylate CREB in vitro, these results alone do not provide evidence that phosphorylation may occur in vivo. In an effort to link GM-CSF-induced pp90RSK activation and CREB phosphorylation toegr-1 expression, we performed transfection experiments using the egr-1 reporter construct and kinase-defective pp90RSK (RSK KD). We previously showed that the −116 CAT/egr-1promoter construct is induced 3-fold in response to GM-CSF stimulation in TF-1 cells, and that the CRE contained within this region is required for maximal transcriptional activation.9 The −116 nucleotide egr-1 promoter construct containing the chloramphenicol acetyltransferase (CAT) gene was cotransfected with expression vectors containing wild-type pp90RSK (RSK WT), kinase-defective (K112/464R) pp90RSK, or empty vector control pcDNA3. No significant differences in GM-CSF-induced reporter activity were observed on cotransfection of the −116 CAT egr-1 ...
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Study Flashcards On 6-04 msk/derm/vasc at Cram.com. Quickly memorize the terms, phrases and much more. Cram.com makes it easy to get the grade you want!
Find all books from Icon Health Publications James N Parker Philip M Parker - The Official Parents Sourcebook on Coffin-Lowry Syndrome: A Revised and Updated Directory for the Internet Age. At find-more-books.com you can find used, antique and new books, COMPARE results and immediately PURCHASE your selection at the best price. 9780497009564
Multiple myeloma is an entity of cytogenetically and genetically heterogenous plasma cell neoplasms. Despite recent improvement in the treatment outcome of multiple myeloma by novel molecular-targeted chemotherapeutics, multiple myeloma remains incurable. The identification of a therapeutic target molecule in which various signaling for cell-survival converge is a core component for the development of new therapeutic strategies against multiple myeloma. RSK2 is an essential mediator of the ERK1/2 signaling pathway for cell survival and proliferation. In this study, we discovered that RSK2Ser227, which is located at the N-terminal kinase domain and is one site responsible for substrate phosphorylation, is activated through phosphorylation regardless of the type of cytogenetic abnormalities or upstream molecular signaling in all 12 multiple myeloma-derived cell lines examined and 6 of 9 patient-derived CD138-positive primary myeloma cells. The chemical inhibition of RSK2Ser227 by BI-D1870 or gene ...
294370448 - EP 1053316 A1 2000-11-22 - NUCLEIC ACIDS PROVIDED FOR MODULATING CELLULAR ACTIVATION - [origin: WO9940187A1] The invention relates to nucleic acids, the derivatives thereof and to sequence specific binding substances which inhibit the expression of the CD30-antigen and/or of the ribosomal S6 kinase pp90rsk3. The invention also relates to pharmaceutical compositions which contain such nucleic acids, and to the utilization of such nucleic acids for modulating cellular activation, suppressing and preventing immunodysregulations, reducing the virus burden, and for eradicating CD30+ and/or pp90rsk3+ cells and the tumors thereof.[origin: WO9940187A1] The invention relates to nucleic acids, the derivatives thereof and to sequence specific binding substances which inhibit the expression of the CD30-antigen and/or of the ribosomal S6 kinase pp90rsk3. The invention also relates to pharmaceutical compositions which contain such nucleic acids, and to the utilization of such nucleic acids for modulating
MSK health (upper extremity/neck), rehab and surgical interventions for MSK disorders, pain and disability, work-related risks, interventions and work disability, KT, gender ...
MSK2 (RPS6KA4) cloned gene : ORF from ATG to Stop, in pUNO1 expression plasmid selectable in E.coli and mammalian cells. Fully sequenced.
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by MSK Australia , Aug 22, 2018 , Lower Limb. CLINICAL INFORMATION 1/52 history of calf pain post take off with pain on resisted plantar flexion. ULTRASOUND FINDINGS A focal tear involving the lateral intramuscular aponeurosis of the Soleus muscle is noted. This is classed as a Grade 2 strain as there is ...
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Ribosomal s6 kinase 2 is a growth factor activated serine/threonine kinase and member of the ERK signaling pathway. Mutations in the Rsk2 gene cause Coffin-Lowry syndrome, a rare syndromic form of intellectual disability. The Rsk2 KO mouse model was shown to have learning and memory defects. We focused on the investigation of the emotional behavioral phenotype of Rsk2 KO mice mainly in the IntelliCage. They exhibited an anti-depressive, sucrose reward seeking phenotype and showed reduced anxiety. Spontaneous activity was increased in some conventional tests. However, KO mice did not show defects in place learning, working memory and motor impulsivity. In addition, we found changes of the monoaminergic system in HPLC and qRT-PCR experiments. Taken together, RSK2 not only plays a role in cognitive processes but also in emotional and reward-related behaviors. ...
Data presented in this study reveal that the MAPK pathway functions in a melanoma cell-specific way to negatively regulate the activity of proapoptotic Bcl-2 family protein Bad. Unlike in normal human melanocytes, Bad is inactivated through hyperactivation of the MEK/ERK/RSK signaling module, and inhibiting this pathway effectively induces apoptotic cell death. Taken together, our findings indicate that constitutive activation of MEK/ERK/RSK signaling and sustained Bad inactivation provide a tumor-specific survival mechanism for melanoma cells.. Constitutive activation of MAPK signaling is a hallmark of many human cancers, including breast and colon cancers and melanoma (1 , 3 , 39 , 46) . Constitutive activation of both MEK and MAPK was demonstrated in melanoma but not in benign nevi (2 , 8) . Expression of CA MEK in immortalized melanocytes promotes tumor formation in nude mice (8) . Recently, a high incidence of activating mutations in B-Raf, an upstream activator of the MEK/ERK signaling, ...
Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a protein that is similar to a serine/threonine kinase in C. elegans which is involved in axonal elongation. The structure of this protein is similar to the C. elegans protein in that both proteins have an N-terminal kinase domain, a central proline/serine rich (PS) domain, and a C-terminal (C) domain. The gene is located within the Smith-Magenis syndrome region on chromosome 17. Alternatively spliced transcript variants encoding the same protein have been identified. [provided by RefSeq, Dec 2008 ...
On page 115, Ku and Omary add one more function to keratins expanding repertoire. In addition to acting as a structural protein in liver cells, keratin 8 (K8) apparently absorbs excess phosphorylation during stress and thus reduces the likelihood of apoptosis.. Humans who carry a G61C polymorphism in K8 are predisposed to liver disease when exposed to insults such as infection. Unlike keratin-associated disorders in skin, these K8 variants do not appear to cause disease directly by decreasing the mechanical strength of cells. In fact, Ku and Omary found that mouse hepatocytes expressing G61C had normal mechanical strength, suggesting that the G61C polymorphism was affecting another stress response process.. G61C interfered with phosphorylation at serine-73 (S73), which is one of two sites in K8 that are phosphorylated by stress-activated kinases during apoptosis. When stress kinases were activated, cells expressing G61C or S73A K8 proteins were more likely to die than those with wild-type K8. ...
2014-11-16 15:10:12 MSK] TransferWatcher: transfer starting: Upload UUID "d865391b-cf21-42d6-a04c-e1b32897c1af" random_1_24 Nothing [2014-11-16 15:10:12 MSK] TransferWatcher: transfer starting: Upload UUID "d865391b-cf21-42d6-a04c-e1b32897c1af" random_1_24 Nothing [2014-11-16 15:10:13 MSK] TransferWatcher: transfer finishing: Transfer {transferDirection = Upload, transferUUID = UUID "d865391b-cf21-42d6-a04c-e1b32897c1af", transferKey = Key {keyName = "f91971893f882086488ca244c7c9e60a5ca23e088a95c171c21e40327de3278b", keyBackendName = "SHA256E", keySize = Just 3145728, keyMtime = Nothing, keyChunkSize = Nothing, keyChunkNum = Nothing}} [2014-11-16 15:10:13 MSK] TransferWatcher: transfer finishing: Transfer {transferDirection = Upload, transferUUID = UUID "d865391b-cf21-42d6-a04c-e1b32897c1af", transferKey = Key {keyName = "f91971893f882086488ca244c7c9e60a5ca23e088a95c171c21e40327de3278b", keyBackendName = "SHA256E", keySize = Just 3145728, keyMtime = Nothing, keyChunkSize = Nothing, keyChunkNum = ...
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