Panoply™ Human GHR Knockdown Stable Cell Line

Name: Panoply™ Human GHR Knockdown Stable Cell Line
SKU: CSC-DC006247
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CSC-DC006247

Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR

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Gene Information

Cat. No.	CSC-DC006247
Description	Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free.
Target Gene	GHR
Host Cell	HEK293 (Hela and other cell types are also available)
Host Cell Species	Homo sapiens (Human)
Applications	(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models
Size	>1 × 10⁶ cells / vial
Stability	Validated for at least 10 passages
Validation	Real-Time RCR
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid Nitrogen
Shipping	Dry Ice

Mycoplasma	Negative
Format	One frozen vial containing millions of cells
Storage	Liquid nitrogen
Safety Considerations	The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship	Dry ice

Gene Name	GHR growth hormone receptor [ Homo sapiens ]
Gene Symbol	GHR
Synonyms	GHBP
Gene ID	2690
Uni Prot ID	P10912
m RNA Refseq	NM_000163.4
Protein Refseq	NP_000154.1
Chromosome Location	5p13-p12
Function	SH2 domain binding; growth factor binding; growth hormone receptor activity; peptide hormone binding; proline-rich region binding; protein binding; protein homodimerization activity; protein kinase binding; protein phosphatase binding;
Pathway	Androgen Receptor Signaling Pathway, organism-specific biosystem; Cytokine Signaling in Immune system, organism-specific biosystem; Cytokine-cytokine receptor interaction, organism-specific biosystem; Cytokine-cytokine receptor interaction, conserved biosystem; Endochondral Ossification, organism-specific biosystem; Growth hormone receptor signaling, organism-specific biosystem; Immune System, organism-specific biosystem;
MIM	600946

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Growth hormone (GH) deficiency in adults is associated with fatty liver disease and several features of the metabolic syndrome. Conversely, obesity is characterized by impaired GH function. Here, researchers aimed to clarify hepatic GH signaling and its metabolic consequences in nonalcoholic fatty liver disease. In humans, GHR and IGF-1 levels were measured in liver samples from 29 obese patients with nonalcoholic steatohepatitis (NASH) or simple steatosis. The cellular effects of GH on insulin signaling were investigated in GH receptor (GHR) knockdown HepG2 cells. Hepatic IGF-1 expression levels reflecting GH action were significantly lower and fasting glucose concentrations were higher in patients with NASH than in patients with simple steatosis. GHR knockdown in hepatocytes resulted in hyperglycemic output, manifested by decreased glycogen content, increased gluconeogenesis, and diminished insulin signaling. These data suggest that GH signaling is diminished in the liver of NASH patients and is associated with decreased hepatic insulin sensitivity and metabolic activity. Reduced hepatic GH activity may contribute to insulin resistance in obese NASH patients.

Insulin signaling activity in hepatocytes was assessed by quantifying Akt phosphorylation (pAKT). As shown in Figure 1, compared with non-silenced control HepG2 cells, Akt phosphorylation at threonine 308 was significantly reduced by 84 ± 9%, and phosphorylation at serine 473 was significantly reduced by 75 ± 7% in GHR knockdown cells. Incubation of GHR knockdown cells with 200 µg/ml IGF-1 for 24 hours did not eliminate the negative effects of Akt phosphorylation in GHR-inhibited cells. G6Pase M-RNA levels were significantly increased by 57 ± 20% in GHR-inhibited cells. Expression levels were also significantly higher in GHR-inhibited cells pre-incubated with IGF-1. Supplementation with IGF-1 significantly increased G6Pase expression in both GHR knockdown and control cells. PC and PCK1 M-RNA levels were higher in GHR knockdown cells than in control cells, but this did not reach statistical significance. The M-RNA expression levels of DGAT2, PPARγ, PPARα, SREBP1c, CPT1, FAS, and SCD-1 were similar between GHR knockdown cells and control cells.

Figure 1. pAKT/AKT in GHR-knockdown cells. (Rufinatscha K, et al., 2018)

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