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Prkcd Mouse shRNA Plasmid (Locus ID 18753)

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SKU
TG513052
Prkcd - Mouse, 4 unique 29mer shRNA constructs in retroviral GFP vector, 5µg of each construct provided
  $883.00
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Specifications
Specifications
Product Data
Locus ID 18753
Synonyms AI385711; D14Ertd420e; Pkcd; PKCdelta; PKCd
Vector pGFP-V-RS
E. coli Selection Kanamycin
Mammalian Cell Selection Puromycin
Format Retroviral plasmids
Components Prkcd - Mouse, 4 unique 29mer shRNA constructs in retroviral GFP vector(Gene ID = 18753). 5µg purified plasmid DNA per construct
29-mer scrambled shRNA cassette in pGFP-V-RS Vector, TR30013, included for free.
RefSeq BC051416, NM_001310682, NM_011103, NM_011103.1, NM_011103.2, NM_011103.3
UniProt ID P28867
Summary Calcium-independent, phospholipid- and diacylglycerol (DAG)-dependent serine/threonine-protein kinase that plays contrasting roles in cell death and cell survival by functioning as a pro-apoptotic protein during DNA damage-induced apoptosis, but acting as an anti-apoptotic protein during cytokine receptor-initiated cell death, is involved in tumor suppression, is required for oxygen radical production by NADPH oxidase and acts as positive or negative regulator in platelet functional responses. Negatively regulates B cell proliferation and also has an important function in self-antigen induced B cell tolerance induction. Upon DNA damage, activates the promoter of the death-promoting transcription factor BCLAF1/Btf to trigger BCLAF1-mediated p53/TP53 gene transcription and apoptosis. In response to oxidative stress, interact with and activate CHUK/IKKA in the nucleus, causing the phosphorylation of p53/TP53. In the case of ER stress or DNA damage-induced apoptosis, can form a complex with the tyrosine-protein kinase ABL1 which trigger apoptosis independently of p53/TP53. In cytosol can trigger apoptosis by activating MAPK11 or MAPK14, inhibiting AKT1 and decreasing the level of X-linked inhibitor of apoptosis protein (XIAP), whereas in nucleus induces apoptosis via the activation of MAPK8 or MAPK9. Upon ionizing radiation treatment, is required for the activation of the apoptosis regulators BAX and BAK, which trigger the mitochondrial cell death pathway. Can phosphorylate MCL1 and target it for degradation which is sufficient to trigger for BAX activation and apoptosis. Is required for the control of cell cycle progression both at G1/S and G2/M phases. Mediates phorbol 12-myristate 13-acetate (PMA)-induced inhibition of cell cycle progression at G1/S phase by up-regulating the CDK inhibitor CDKN1A/p21 and inhibiting the cyclin CCNA2 promoter activity. In response to UV irradiation can phosphorylate CDK1, which is important for the G2/M DNA damage checkpoint activation. Can protect glioma cells from the apoptosis induced by TNFSF10/TRAIL, probably by inducing increased phosphorylation and subsequent activation of AKT1. Can also act as tumor suppressor upon mitogenic stimulation with PMA or TPA. In N-formyl-methionyl-leucyl-phenylalanine (fMLP)-treated cells, is required for NCF1 (p47-phox) phosphorylation and activation of NADPH oxidase activity, and regulates TNF-elicited superoxide anion production in neutrophils, by direct phosphorylation and activation of NCF1 or indirectly through MAPK1/3 (ERK1/2) signaling pathways. May also play a role in the regulation of NADPH oxidase activity in eosinophil after stimulation with IL5, leukotriene B4 or PMA. In collagen-induced platelet aggregation, acts a negative regulator of filopodia formation and actin polymerization by interacting with and negatively regulating VASP phosphorylation. Downstream of PAR1, PAR4 and CD36/GP4 receptors, regulates differentially platelet dense granule secretion; acts as a positive regulator in PAR-mediated granule secretion, whereas it negatively regulates CD36/GP4-mediated granule release. Phosphorylates MUC1 in the C-terminal and regulates the interaction between MUC1 and beta-catenin. The catalytic subunit phosphorylates 14-3-3 proteins (YWHAB, YWHAZ and YWHAH) in a sphingosine-dependent fashion. Phosphorylates ELAVL1 in response to angiotensin-2 treatment (By similarity).UniProtKB/Swiss-Prot Function
shRNA Design These shRNA constructs were designed against multiple splice variants at this gene locus. To be certain that your variant of interest is targeted, please contact techsupport@origene.com. If you need a special design or shRNA sequence, please utilize our custom shRNA service.
Storage Store at -20°C
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Documents
Resources

file-alt Citations

Protein Kinase C Delta restrains growth in ACTH-secreting pituitary adenoma cells
Gentilin, Di Pasquale, Gagliano et al
Mol. Cell. Endocrinol. (2015)
Cited by 13
AI Summary: OriGene’s PRKCD shRNA plasmid was used to silence PRKCD expression in AtT-20/D16v-F2 cells, enabling the study of PRKCD’s role in regulating cell growth and behavior in ACTH-secreting pituitary adenoma cells.
Snippet: 2.2. Transfection with PRKCD shRNA. Cells were transfected with PRKCD shRNA plasmid (OriGene, Rockville, MD, USA), by using Nucleofector II (Amaxa, Gaithersburg, MD, USA) according to the manufacturer's protocols, as previously reported (Gentilin et al., 2013a ... Cite SaveSaving
Resveratrol inhibits NLRP3 inflammasome activation by preserving mitochondrial integrity and augmenting autophagy
Chang, Ka, Hsu et al
J. Cell. Physiol. (2014)
Cited by 217
AI Summary: OriGene’s shRNA plasmids targeting PKCδ and a scrambled control (OriGene Technologies, Inc.) were used to generate stably transfected cell lines, enabling the study of PKCδ’s role in NLRP3 inflammasome activation in this research.
Snippet: established by stable transfection using shRNA plasmids targeting PKCδ and a scrambled sequence, respectively (OriGene Technologies, Inc., Rockville, MD). IL-1β secretion and caspase-1 activation For IL-1β secretion and caspase-1 activation in Fig. ... Cite SaveSaving
The Hypoxia-Inducible Epigenetic Regulators Jmjd1a and G9a Provide a Mechanistic Link between Angiogenesis and Tumor Growth
Ueda, Ho, Lee et al
Mol. Cell. Biol. (2014)
AI Summary: OriGene's retrovirally expressed shRNAs were used in this study to specifically knock down gene expression, enabling the researchers to investigate the roles of Jmjd1a and G9a in tumor growth and angiogenesis.
Snippet: Day 21 (WT: n=11, Jmjd1a KO: n=17). 202 203 shRNA Experiments 204 Specific knockdown of mRNA expression was performed using retrovirally expressed shRNAs 205 (OriGene Technologies, MD, USA). Recombinant viruses were prepared by co-transfection of ... Cite SaveSaving
Klotho sensitizes human lung cancer cell line to cisplatin via PI3k/Akt pathway
Wang, Chen, Huang et al
PLoS ONE (2013) 8 (2), e57391 DOI: 10.1371/journal.pone.0057391
Cited by 76
AI Summary: OriGene contributed to this study by providing plasmids used for manipulating klotho expression in human lung cancer cell lines, enabling the investigation of klotho's role in sensitizing cells to cisplatin via the PI3K/Akt pathway.
Snippet: All cell lines were maintained in RPMI 1640 (Life Technologies, Inc., Gaithersburg, MD) containing 10% fetal bovine serum (FBS) (Life Technologies, Inc.), 100 U/mL penicillin, 100 U/mL streptomycin, 2 mM ... All plasmids were purchased from the OriGene (Rockville, MD, USA).
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Showing 1-4 of 4 papers.
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