SGK1 Antibodies

Serine/threonine-protein kinase Sgk1 (SGK1)

Serine/threonine-protein kinase that is involved in the regulation of a wide array of ion channels, membrane transporters, mobile enzymes, transcription factors, neuronal excitability, cell growth, proliferation, survival, migration and apoptosis. Plays an essential role in cellular stress response.

Up-regulates Na(+) channels: SCNN1A/ENAC, SCN5A and ASIC1/ACCN2, K(+) channels: KCNJ1/ROMK1, KCNA1-5, KCNQ1-5 and KCNE1, epithelial Ca(2+) channels: TRPV5 and TRPV6, chloride channels: BSND, CLCN2 and CFTR, glutamate transporters: SLC1A3/EAAT1, SLC1A2 /EAAT2, SLC1A1/EAAT3, SLC1A6/EAAT4 and SLC1A7/EAAT5, amino acid transporters: SLC1A5/ASCT2, SLC38A1/SN1 and SLC6A19, creatine transporter: SLC6A8, Na(+)/dicarboxylate cotransporter: SLC13A2/NADC1, Na(+)-dependent phosphate cotransporter: SLC34A2/NAPI-2B, glutamate receptor: GRIK2/GLUR6. Stimulates sodium transfer into epithelial cells by improving the stability and expression of SCNN1A/ENAC.

Gene Information

Human
Gene Name:	SGK1
Uniprot:	O00141
Entrez:	6446

Family

Belongs to:
protein kinase superfamily

Alternative Names

EC 2.7.11; EC 2.7.11.1; serine/threonine protein kinase SGK; serine/threonine-protein kinase Sgk1; serum/glucocorticoid regulated kinase 1; serum/glucocorticoid regulated kinase; Serum/glucocorticoid-regulated kinase 1; SGK; SGK1

Molecular Weight

Mass (kDA):
48.942 kDA

Genomic Context

Human
Location:	6q23.2
Sequence:	6; NC_000006.12 (134169246..134318112, complement)

Tissue Specificity

Expressed in most tissues with highest levels in the pancreas, followed by placenta, kidney and lung. Isoform 2 is strongly expressed in brain and pancreas, weaker in heart, placenta, lung, liver and skeletal muscle.

Subcellular Localizations

Cytoplasm. Nucleus. Endoplasmic reticulum membrane. Cell membrane. Mitochondrion. The subcellular localization is controlled by the cell cycle, as well as by exposure to specific hormones and environmental stress stimuli. In proliferating cells, it shuttles between the nucleus and cytoplasm in synchrony with the cell cycle, and in serum/growth factor-stimulated cells it resides in the nucleus. In contrast, after exposure to environmental stress or treatment with glucocorticoids, it is detected in the cytoplasm and with certain stress conditions is associated with the mitochondria. In osmoregul

Diseases

• Hypertensive Disease
• Neoplasms
• Malignant Neoplasms
• Kidney Diseases
• Fibrosis
• Diabetes Mellitus
• Inflammation
• Diabetic Nephropathy
• Proteinuria Of Undiagnosed Cause
• Ischemia
• Diabetes Mellitus, Non-insulin-dependent
• Edema
• Hypernatremia

• Injury To Kidney
• Obesity
• Carcinoma
• Hyperglycemia
• Hypertrophy
• Pseudohypoaldosteronism
• Cell Transformation, Neoplastic

Interacting Proteins

• TSC2
• Wnk4

Pathways

• Transport
• Excretion
• Secretion
• Localization
• Cell Proliferation
• Ion Transport
• Pathogenesis
• Cell Growth
• Glucose Transport
• Cell Death
• Cell Cycle
• Gastric Acid Secretion
• Acid Secretion

• Endocytosis
• Translation
• Regulation Of Transport
• Coagulation
• Glomerular Filtration
• Rna Interference
• Amino Acid Transport

PTMs

• Phosphorylation
• Ubiquitination
• Dephosphorylation
• Methylation
• Cleavage

• Carboxylation
• Reduction
• Biotinylation
• Glycosylation
• Acetylation

Research Areas

• Apoptosis
• DNA Repair

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SGK1

Best Uses of the SGK1 Marker

There are many facets of the SGK1 marker, so this article will quickly review the various uses of this protein. We will also look at the SGK3 marker ZINC00319000 and HOTTIP. If you have any queries regarding the SGK1 marker, feel free to ask your comments below! We hope this article can help you make the right choice when purchasing SGK1 antibodies.

SGK1

The SGK1 marker has many applications in biology. It influences a myriad of physiological processes and is involved in the pathophysiology behind many diseases, including hypertension, diabetes, inflammation, autoimmune disease, and tumor growth. Here are some examples of how SGK1 can be used. the SGK1 gene.

This marker has an excellent chance of identifying human cancers. The gene plays a pivotal function in determining the course of cancer. Similarly, in NSCLC patients high levels of SGK1 genes were associated with poorer survival. Tang et. and. recently found that patients with higher level of SGK1 mRNA had shorter OS and lower disease-free survival. found that esophageal squamous cell carcinoma patients with high SGK1 levels had shorter OS and disease-free survival compared to their counterparts with low SGK1.

SGK1 expression is also linked to clinical characteristics of human carcinoma such as stage and metastasis. One study revealed that high SGK1 gene copies were linked to metastasis in high-grade Mullerian adenosarcomas. In another study it was found that high SGK1 gene expression was associated with more advanced tumors, which were more in size, and had worse clinical stage.

The progression of cancer has been associated with SGK1-mediated control of autophagy. It is also involved in the maintenance of the skeletal muscle's homeostasis and the expression of SGK1 reduced proteolysis and enhanced protein synthesis during hibernation. This research has important implications in cancer research. One of the most promising targets in drug development is the SGK1 gene.

SGK3

In this study, a reporter gene was transfected into human keratinocytes. The reporter gene, lef-1, was used to identify cells expressing mutant SGK3. A PI3K-effector, called PDK1, was also utilized to activate SGK3 within the keratinocytes that were transfected. The results of this study prove that SGK3 plays a role in signaling in the proliferation and differentiation of cells.

The immunoblot assays are used to measure the expression levels of SGK3. These tests are available to all scientists across the globe. This is a valuable resource for scientists who are looking for an approach to measure SGK3 levels in their research. The boster protein capture technique is highly accurate and reproducible. The results were consistent. It offers many advantages and should be of interest to researchers across the globe.

Proteinuria has been linked with the expression of SGK3 through nephritis caused by ADR in mouse models. Mice were given ADR to cause nephritis. The urinary albumin/creatinine was determined prior to and after the injection. Immunoblot analysis confirmed the presence of SGK3 and nephrin in kidney tissues. In addition, immunohistochemical staining demonstrated an increased expression of nephrin as well as SGK3 in glomeruli.

Hair follicle development in heterozygous mouse lacking SGK3 was affected. In addition, their follicles showed abnormal organization. The results of adult mice with the KO hair follicle defect in their follicles were not particularly impressive. However, further research is required to determine whether the defect has a greater impact on hair cycle defects. The initial defect was limited to the hair follicles. However, the interfollicular epidermis was normal.

ZINC00319000

There are a variety of biological functions regulated by SGK1 It is involved in the pathophysiology of a variety of diseases. It influences the growth and spread of cancer cells and also hypertension, autoimmune illness and inflammation, just to name several. But what exactly is this protein doing? What are the best uses for SGK1 markers? Let's look!

SGK1 is involved in the development of nearly all tumors. It can be used as a biomarker in order to identify and predict the future outcome. This review outlines the scientific successes of SGK1 research in the field of cancer, and highlights the challenges associated with its use in clinical trials. It examines its biological and clinical functions and provides information that can be beneficial in the development of new cancer treatments.

The SGK1 gene can be located in the brain, liver and lung. It is possible to detect SGK1 in these patients could suggest a favorable or bad prognosis. It is important to note that this marker isn't yet specific for cancer. Clinical trials can only be conducted if it is confirmed as a biomarker.

In addition to regulating tumor-related activities, SGK1 also regulates the differentiation of T helper 17 cells as well as regulatory T cells. This protein regulates the activity of macrophages that are tumor-associated (also called M2-like macrophages). These cells also express arginase 1, or Arg1.

HOTTIP

HOTTIP, a long-non-coding RNA that regulates the SGK1 gene during pancreatic cancer. HOTTIP is involved in many complexes, such as MLL1 WDR5, PRC2 and MLL1 which is different from its cousin HOTAIR. These interactions are not completely understood. However they do appear to be related. Here, we discuss some recent research findings regarding HOTTIP and SGK1 expression.

HOTTIP is thought to be an oncogene since it regulates SGK1, a steroidshormone. It is involved in CRC-related cells by preventing proliferation and migration, and it causes apoptosis. HOTTIP is also linked to miRNAs which act as epigenetic regulators. MiRNAs regulate SGK1 expression by inhibiting the expression of SGK1 through its 3'-UTR.

HOTTIP affects gene expression. Researchers transfected Panc1 cells with siRNA or siHOTTIP. They then examined the results using an Illumina Human 3 HT12 array. Transfection of cells with siHOTTIP resulted in increased expression of 514 genes and decreased expression of 757 genes. HOTTIP regulates genes involved in cell growth, survival, and migration. HOTTIP could regulate genes that are related to cell growth, differentiation, and metabolism.

SGK1 is involved in the development and differentiation of certain proteins. Through the use of lentiviral-based sRNA, the abolition of SGK1 expression reduced colony formation and reduced the expression of membranous E-cadherin in CRC cell lines. If the reexpression of SGK1 is successful, cells may show decreased growth rates and a higher degree of differentiation.

SGK1 Marker

SGK1 is a phosphorylation of the lysine-specific methyltransferase (KMT2D) enzyme. This blocks KMT2D function and affects the methylation of lysine4 on histone H3 (H3K4). This compound stabilizes the SGK1 protein while causing only slight changes in its structure. It could be used as a scaffold for the development of SGK inhibitions, but further studies are required.

Despite being involved in almost all types of tumors, SGK1 may function as biomarker to aid in cancer diagnosis and prognosis. This review reviews the scientific achievements of cancer research based on SGK1. It also discusses the clinical challenges of the SGK1-based cancer diagnosis. This review also analyzes the biochemical mechanism of SGK1 and its role in the metabolism of tumors. It could be a new cancer therapy target.

SGK1 is an important biomarker of cancer resistance. Studies have shown that SGK1 levels in prostates with resistance to castration carcinoma are higher than those in CRPC cells with tamoxifen resistance. Furthermore, SGK1 has been shown to play a role in the development of CRPC. SGK1 also played a key role in the development and maintenance of resistance to chemotherapy in rhabdomyosarcoma.

Autophagy mediated by SGK1 has been implicated in the process of metabolizing cancer, because it is crucial for cancer progression. Combined with radiation therapy, inhibition of SGK1 can be an effective antitumor strategy. Andres-Mateos et al. It was discovered that inhibition of SGK1 results in a decrease in the unsaturated fatty acid synthesis in cancer cells, and an increase in the caspase-3 activity.

SGK3 construction

The SGK3 gene is likely to be expressed in tumor cells. Recent studies suggest that SGK3 expression plays a role in tumor cell infiltration and migration. This gene could be a candidate for drug development. The pEGFP-N1-SGK3 construct has been successfully transfected into MDA-MB-231 cells. It was also observed that cells transfected by pEGFP-N1-SGK3 had a longer time to double than their N1-sibling counterparts.

Despite the lack of evidence direct however, the SGK3 overexpression group had greater rates of migration compared to the other groups. After 24 hours, SGK3 cells had almost no visible scratch marks when compared with the other two groups. Overexpressing SGK3 cells had an apoptotic percentage that was lower cells than the other two groups. They also had lower levels than the N1 or 231 groups of BRMS1.

The SGK3 construct not only improved multiplication and mobility, but also altered the expression of the protein BRMS1, which is involved in the process of tumor metastasis and invasion. While the increase in BRMS1 levels was not statistically significant in this particular case however, a significantly increased level of SGK3 in tumor cells led to a better survival of cells. These results support the hypothesis of SGK3 in Boster bio having the ability to increase tumor invasion and migration.

Nephrin is a protein that binds to ubiquitin-proteasomes. However, SGK3 can be inhibited to activate Nedd4-2 which regulates the degradation of nephrin via ubiquitin. This protein is also involved in nephrin-mediated signaling conduction. Although the role of nephrin has not been fully known, its presence in podocytes has significant physiological benefits for renal cell growth and function.