SEC23A Antibodies

Protein transport protein Sec23A (SEC23A)

Part of the coat protein complex II (COPII) which promotes the formation of transport vesicles from the endoplasmic reticulum (ER). The coat has two main purposes, the physical deformation of the endoplasmic reticulum membrane into vesicles along with the choice of cargo molecules for their transport to the Golgi complex.

Required for the translocation of insulin-induced glucose transporter SLC2A4/GLUT4 into the cell membrane (By similarity). .

Gene Information

Human
Gene Name:	SEC23A
Uniprot:	Q15436
Entrez:	10484

Family

Belongs to:
SEC23/SEC24 family

Alternative Names

CLSD; MGC26267; protein transport protein Sec23A; Sec23 (S. cerevisiae) homolog A; Sec23 homolog A (S. cerevisiae); SEC23-related protein A

Molecular Weight

Mass (kDA):
86.161 kDA

Genomic Context

Human
Location:	14q21.1
Sequence:	14; NC_000014.9 (39031919..39103235, complement)

Tissue Specificity

Ubiquitously expressed.

Subcellular Localizations

Cytoplasmic vesicle, COPII-coated vesicle membrane; Peripheral membrane protein; Cytoplasmic side. Endoplasmic reticulum membrane; Peripheral membrane protein; Cytoplasmic side. Cytoplasm, cytosol. Enriched at endoplasmic reticulum exit sites, also known as transitional endoplasmic reticulum (tER).

Diseases

• Dysplasia
• Stomatitis
• Vesicular Stomatitis
• Craniofacial Abnormalities
• Endoplasmic Reticulum Stress
• Neoplasm Metastasis
• Congenital Dyserythropoietic Anemia
• Congenital Dyserythropoietic Anemia, Type Ii
• Fibrosis
• Neoplasms
• Hereditary Diseases

• Anemia
• Pathological Dilatation
• Cystic Fibrosis
• Williams Syndrome
• Malignant Neoplasm Of Breast
• Orbital Separation Excessive

Interacting Proteins

• CDK16
• SEC24C

Pathways

• Transport
• Secretion
• Secretory Pathway
• Protein Transport
• Localization
• Golgi Localization
• Protein Secretion
• Protein Folding
• Intracellular Transport
• Cell Proliferation
• Cellular Homeostasis
• Fertilization
• Proteolysis

• Erythrocyte Development
• Spermatogenesis
• Cytokinesis
• Lateral Growth
• Chondrocyte Development
• Lipid Homeostasis
• Cell Differentiation

PTMs

• Cleavage

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SEC23A

Best Uses Of The SEC23A Marker From Boster Bio

As the name implies, SEC23A is a gene that is found on the surface of many cells. Boster provides high-affinity antibodies for the SEC23A marker. These antibodies are cited widely and have been validated in multiple assays including Western Blotting, Immunohistochemistry, and ELISA. Listed below are some of the most commonly used SEC23A antibodies.

Anti-SEC23A Marker

The Anti-SEC23A Marker in the Boster Bio catalog is A05287-1 and reacts with Human. This antibody has been tested for use in IHC, WB, IP and Flow Cytometry. This reagent is supplied as 100ul Liquid. The antibody is tested on human and mouse samples. It is highly specific for SEC23A. It is available in Liquid form or as a powder for ELISA.

Purified Sec24C binds to p58 and APP, but only with low affinity. It may cooperate with recombinant proteins in order to form vesicles or select cargo molecules. Both first and second models invoke a non-COPII protein required for efficient vesicle formation. The third model suggests the involvement of other COPII subunits.

This reagent also stimulates budding by binding recombinant mammalian COPII proteins to the microsomal membrane. This reagent was fractionated by SDS-PAGE and transferred to a polyvinylidene difluoride membrane. The bound proteins were analyzed by SDS-PAGE using the indicated antibodies. The Anti-SEC23A Marker in Boster Bio is highly specific for Sec23A and PS1 proteins.

Applications

The SEC23A gene is a candidate gene for MTC. Researchers at the Takara Institute for Medical Research used a SEC23A knockout in cells to test this candidate gene. The results showed that SEC23A gave the highest AUC value (0.636). The AUC value was also higher for a score model developed using a five-year time interval compared to one-year AUC and three-year AUC.

SEC23A has been implicated in the progression of bladder cancer. Overexpression of SEC23A was successful in constructing human bladder cancer cell line T24. Western blot assays revealed that silencing the gene reduced the migration and invasion capacity of T24-shSEC23A cells. In contrast, overexpression of the gene enhanced migration and invasion capacities. The findings support the importance of SEC23A in the progression of bladder cancer.

In addition to its aforementioned uses, SEC23A has been identified as an mRNA target of miR-375 in human prostatic cancer cells. Immunoblotting and immunohistochemistry analysis revealed that SEC23A protein expression decreased in MTC C-cells and TT cells transfected with miR-375 mimics. However, these studies also show that miR-375 negatively correlates with SEC23A expression. This suggests that the miR-375 inhibitor agonist can counteract SEC23A action by inhibiting strong oncogenes.

Another study revealed that SEC23A was associated with a higher number of CD4+ T cells than CD8+ T cells. This result supports the concept that SEC23B and SEC23A are interdependent and can compensate for one another. Furthermore, these proteins are expressed in T cells from human and mice donors, and this may help explain the absence of CDAII-associated immunodeficiency.

COPII translocation has been linked with the relocation of the Golgi membranes. Moreover, YFP-Sec23A accumulates above the nucleus. This accumulation of structures above the nucleus is consistent with the reorganization of the cell periphery. This observation confirms the concept of COPII-containing structures in cells. It also shows that ER export sites increase during the interphase of the cell cycle, and YFP-SEC23A can be visualized throughout the cell's depth.

Specificity

The SEC23A gene is a known oncogene, but its exact role in the progression of human cancers is not yet understood. SEC23A expression has been found to be an independent poor prognostic factor in bladder cancer. As such, SEC23A is likely an oncogene. However, future studies are needed to clarify the biological processes regulated by SEC23A and determine its role in cancer initiation and progression.

The dSec16 domain is located at the N-terminus of the protein. The marker detects dSec16 only in cells that contain the mutant SEC23A. However, this mutant lacks the dSec16 domain, which makes it a poor marker. It also shows poor specificity compared with wild-type Sar1 because the dSec16 does not uncoat.

The SEC23A gene is associated with TMB, MSI, stemness score, drug sensitivity, and TME. It also correlates with survival analysis and KM. Further, it shows a good correlation with TGF-BETA. Further, SEC23A is correlated with other KEGG genes. And SEC23A expression correlates with MEF2A and Hspa12a.

The SEC23A gene is a highly conserved protein in the ER. However, there are several cases when a depleted cell has a mutant SEC23A gene. In this case, a mutation of Sar1 or SEC23A leads to a phenotype that is similar to the wild-type SEC23A marker. It also plays an important role in the regulation of secretion.

A human bladder cancer T24 cell line was obtained from the China Center for Type Culture Collection. Cells were maintained in a 37deg C incubator in 5% CO2. A sh-RNA sequence was designed to target SEC23A. The target was 5'-GGAAGCTACAAGATTGT-3'. Sangon Biotech Co. produced shSEC23A lentivirus particles. When applied to bladder cancer cells, these lentivirus particles showed a very high specificity for the marker.

The SEC23A gene is upregulated after CREB3L2/BBF2H7 activates it. TGF-b and a-SMA also upregulate SEC23A and Sec24D. CREB3L2/BBF2H7 depletion decreased both Sec23A and SEC24D expression in dermal fibroblasts. These results are consistent with those observed in the control group.

Availability

This boster bio anti-SEC23A antibody has been tested for use in IHC, ICC, WB, and Flow Cytometry. It reacts with both Mouse and Human cells. The antibody is available with a reference price of $62.

The miR-375 targets SEC23A and YAP1 in PC cell lines and inhibits their expression. Together, these miRs are therapeutic targets for overcoming chemo-resistance in mCRPC stage. These two genes are important for predicting and monitoring sensitivity to docetaxel. This research indicates that miR-375 is a potential drug target for cancer cells.