Rasd1 Antibodies

Dexamethasone-induced Ras-related protein 1 (Rasd1)

Small GTPase.

Negatively regulates the transcription regulation activity of the APBB1/FE65-APP complex via its interaction with APBB1/FE65 (By similarity).

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Gene Information

Mouse
Gene Name:	Rasd1
Uniprot:	O35626
Entrez:	19416

Family

Belongs to:
small GTPase superfamily

Alternative Names

Activator of G-protein signaling 1; AGS1ras-related protein; DEXRAS1dexamethasone-induced Ras-related protein 1; MGC:26290; RAS, dexamethasone-induced 1

Molecular Weight

Mass (kDA):
31.684 kDA

Genomic Context

Mouse
Location:	11|11 B1.3
Sequence:	11;

Tissue Specificity

Expressed in brain, heart, kidney and liver.

Diseases

• Malignant Neoplasms
• Neoplasms
• Pertussis
• Melanoma
• Malignant Neoplasm Of Breast
• Carcinoma
• Pituitary Diseases
• Mammary Neoplasms
• Oligodendroglioma
• Adenomatous Polyposis Coli
• Bone Neoplasms
• Multiple Myeloma
• Cell Invasion

• Neurotoxicity Syndromes
• Neoplasm Metastasis
• Oncogene Activation Process
• Hypoxia
• Fibrosarcoma
• Headache
• Renal Cell Carcinoma

Pathways

• Secretion
• Cell Cycle
• Hormone Secretion
• Cell Proliferation
• Localization
• Methylation
• Cell Growth
• Dna Hypomethylation
• Proteolysis
• Immune Response
• Cell Division
• Regulation Of Corticotropin Secretion
• Sensitization

• Reverse Transcription
• Embryo Implantation
• Corticotropin Secretion
• Response To Desiccation
• Secretory Pathway
• Circadian Rhythm
• Lactation

PTMs

• Phosphorylation
• Methylation

• Nitrosylation
• Prenylation

• Ribosylation

Research Areas

• Signal Transduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Rasd1

Best Uses of the RASD1 Marker

This article explains what the RASD1 (a member in the RAS superfamily), is used for. Its function involves inhibiting migration and invading cells and altering the cytoskeletal structure of glioma. It also shows how RASD1 could be used to discover biomarkers. Here are a few examples to show you how RASD1 may help with your research.

RASD1 is a member in the RAS superfamily

RASD1 may be a small GTPase with an oncogenic function. However, evidence for this is contradictory. Overexpression of RASD1 within cancer cell line cells increased osteosarcoma-cell proliferation, but inhibited growth in lung adenocarcinoma, kidney cell carcinoma, breast cancer cell line lines, and renal cell carcinoma. Moreover overexpression of RASD1 did not have any significant effect on proliferation as measured using EdU or CCK8 tests. Similarly, RASD1 expression had no effect in the progression of cells in Lenti–RASD1 cell lines.

A GFP–Rasd1 Lentivirus was used in a recent study for transfecting U87 and D47D cells. In the presence of Rasd1 lentivirus, 90% of the cells expressed GFP fluorescence. The lentivirus mediated stable cell lines also demonstrated that RASD1 was highly efficient.

One of the small GTPases activating a yeast pheromone pathway is RASD1. It is inducible via dexamethasone. It is also linked to the RAS superfamily, small GTPases. Further research is needed to determine the role of this gene in regulating cell metabolism and disease progression.

Overexpression of RASD1 results in reduced vasopressin release and altered actin cytoskeleton. In wound healing assays RASD1 overexpression also decreases glioma cellular migration. Transwell migration assays showed similar effects.

RASD1 is only expressed in AVP-positive neuronal cells, which suggests that it may be expressed at other levels. It was discovered that RASD1 is present in the neuronal cells body, dendrites and axons from control animals. This is a new finding. H-Ras has been identified in axon terminations as well. H-Ras activation consistently has been associated with changes within the axons, such as a decrease AVP contents.

RASD1 is a member a subfamily G proteins, the RAS. It has been shown that it regulates the glucocorticoid systems and has been implicated with metabolic disorders. It is also believed to play a part in circadian rhythms. RASD1 is therefore a candidate to be a drug target. Many types of cancer can be caused by inflammation.

It inhibits migration and invasion

The RASD1 superfamily member is the RASD1 RNA protein. It promotes cell growth and tumor expansion. It can also play an active role in the prevention of abnormal cell growth. Below are some of the best uses for the RASD1 marker. RASD1 may be useful for cancer research and cancer diagnosis, including the detection of leukemia cells.

In nude mice, a intracranial model of glioma and xenografts was established. Coronal sections were used for hematoxylin and eosin staining to assess tumor growth. The tumor volume of the Lenti-Vector group was not significantly different from that of the Lenti-RASD1 group. GFP-labeled cancer cells in Lenti–RASD1 invasive the brain less often than those from Lenti–Vector. Furthermore, the Lenti-RASD1 group also showed less number of invading cells outside the tumor core.

RASD1 overexpression led to lower levels of p–AKT (Thr308), and p–S6 in U87 cells and U251 cell lines. RASD1 was also found to inhibit the AKT/mTOR pathway in glioma cells. But, there is more than meets the eyes with this gene. More research is needed in order to understand the function of this gene and its impact on human cancer cells.

It is important to understand how RASD1 interacts glioma cells in order to determine the role of RASD1 for cancer research. Transfection can be used to express this marker in cells. To express RASD1 into glioma cell glioma, a RASD1 lentivirus (RASD1) was used. This transfection was done according to the manufacturer's instructions. Immunofluorescence and imaging of ligated cytotoxicity confirmed the infection of RASD1-overexpressing cell lines.

Scientists can study disease progression through cell culture using the RASD1 marker. It can be used to distinguish between different types of cancer. It can also be used for detecting the RASD1 proteins in tumors. The RASD1 marker has many other potential uses. It is vital to use the gene for cancer research.

42 astrocytoma tissues from different grades were examined for the expression RASD1 protein. The RASD1 protein level increased significantly in grade II astrocytoma and nontumor brain tissues. Interestingly the RASD1 proteins were not significantly reduced in grade IV glioma tissues. This protein level is especially useful for predicting survival of patients with astrocytoma.

It inhibits AKT/mTOR.

RASD1 is a member of the RAS superfamily of small G-proteins. This gene is involved in cell proliferation and tumor expansion and is often downregulated in cancer. It may also help to prevent aberrant cell development. It can inhibit AKT/mTOR signaling. In some cases, it may even help to prevent tumor formation.

The cytoskeleton reorganization in glioma cellular gliomas was caused by RASD1 expressing too much. This was observed using phalloidin staining. The cells expressing RASD1 showed less aggregation in the actin cytoskeleton of the cell membrane. LentiRASD1 U251 cells showed greater actin-driven projections during cell migration than their nonoverexpressing counterparts.

The authors tested RASD1 in glioma as well as non-glioma cells by using a 2-step cell cycle model. The colony size increased in U251 cells and U87 cells when RASD1 was overexpressed. In the representative images (A) and in the quantitative analysis (B), the Lenti-RASD1 group produced larger colonies than the Lenti-Vector group.

Boster Bio has successfully used this biomarker to test SPOCK1 in its anti-cancer activity. Researchers and patients who are interested in cancer research will reap the benefits of inhibiting the PI3K/AKT/mTOR pathway. It blocks the AKT/mTOR pathway. These are not treatments that work, but they are promising tools in cancer research.

RASD1 offers many benefits. It has been shown in studies to inhibit the AKT/mTOR pathway as well as induce autophagic cell deaths. Inhibiting the RASD1 protein also promotes tumor suppression and autophagy. It promotes AVd production and decreases anti-apoptotic Bcl-2. It also inhibits PI3K/AKT signaling.

ANXA6 regulates autophagy. It increases the expressions Beclin-1 and LC3II/I, by inhibiting PI3K/AKT/mTOR. By inhibiting PI3K/AKT/mTOR, Beclin-1 and P62 are increased. Boster Bio's RASD1 marker blocks the AKT/mTOR pathway.

It alters cytoskeletal organisation in glioma cellular cells

Overexpressions RASD1 result in a reorganization and decrease in migration and invasion rates of glioma cellular cells. F-actin distribution in the cytoplasm was lower and more consolidated in the cell membrane according to phalloidin stained cytoskeleton. Actin-driven protrusions tended to be more diffusely distributed through the cytoplasm.

The RASD1 proteins bind to PINCh2 in FA sites, allowing them to regulate cell invasion and migration. The researchers also discovered that RSU-1 expression is associated with aggressiveness of glioma cells. The role of RSU-1 remains unclear. It is known however that silencing this protein reduces the migration or invasion of cancer cells.

RASD1 affects the cytoskeletal organization of glioma cells, which is a hallmark of this type of tumor. This gene is closely associated with the glioma cell invasion process, but it has not been studied in the central nervous system. It can also affect tumor cells from other organs, but it is associated aggressiveness in the glioma.

RASD1 is necessary for translocation of Ras proteins to the cell membrane and stimulation of protein-protein interactions. Itoprenylation of the protein can decrease its stability. This could contribute to the decreased level of the protein during SL. It is still unclear how this gene affects the growth of tumor cells. Further research is needed. It has been shown in SL to influence the expression of cFos1 (and Nr4a1) genes.

It is known that RASD1 has a wide range of cell functions, including motility and invasion, migration, survival, as well as cellular functions such as migration and invasion. It was also shown that GDF15 is critical in the migration and invasion of glioma cells. It is also associated RASD1 expression which may be tumor-promoting. However, this gene might act as an inhibitor of glioma growth.

The immunofluorescent localisation method was used to assess Rasd1's RNA expression. Both SON and PVN cells expressed the protein. RASD1 is most prominent in the parvocellular region of both PVN, SON. These cells also expressed oxytocin which is a related neuropeptidehormone.