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- Table of Contents
2 Citations
Facts about Alpha-actinin-4.
Probably involved in vesicular trafficking through its association with the CART complex. The CART complex is necessary for effective transferrin receptor recycling but not for EGFR degradation (PubMed:15772161).
Human | |
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Gene Name: | ACTN4 |
Uniprot: | O43707 |
Entrez: | 81 |
Belongs to: |
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alpha-actinin family |
actinin alpha4 isoform; actinin, alpha 4; ACTININ-4; alpha-actinin-4; DKFZp686K23158; F-actin cross-linking protein; focal segmental glomerulosclerosis 1; FSGS; FSGS1; Non-muscle alpha-actinin 4
Mass (kDA):
104.854 kDA
Human | |
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Location: | 19q13.2 |
Sequence: | 19; NC_000019.10 (38647649..38731589) |
Widely expressed.
Nucleus. Cytoplasm. Cell junction. Cytoplasm, cytoskeleton, stress fiber. Localized in cytoplasmic mRNP granules containing untranslated mRNAs. Nuclear translocation can be induced by the PI3 kinase inhibitor wortmannin or by cytochalasin D. Exclusively localized in the nucleus in a limited number of cell lines (breast cancer cell line MCF-7, oral floor cancer IMC-2, and bladder cancer KU-7).
Anti-Actinin Alpha 4 (ACTN4) Marker is a primary antibody which reacts with human and is available from Boster Bio. This antibody has been tested and proven to work in flow cytometry, IP and IF. This boster bio anti-actinin alpha 4 antibody has multiple uses including molecular biology, pharmacology, clinical research, and gene infographics.
The Anti-Actinin Alpha 4 ACT-A4 antibody, catalog number A01975, has been tested for its ability to detect human ACTN4 in flow cytometry. Previously, this antibody had only been tested in IP and Flow Cytometry. However, its use in Flow Cytometry and WB has now expanded to include cell proliferation assays.
ACTN4 is expressed in iEVTs and is required for their migration into decidua. It also plays a vital role in cell invasion. Depletion of ACTN4 inhibits cell migration by disrupting actin filament organization. Inhibition of ACTN4 inhibits villous outgrowth, suggesting that loss of ACTN4 might contribute to preeclamptic placenta pathogenesis.
ACTN4 protein levels were two to threefold higher in LNCaP-AI cells compared to LNCaP-P cells. Knockdown of ACTN4 suppressed cell proliferation in LNCaP cells. ACTN4 knockdown decreased cell proliferation in LNCaP-AI cells. In contrast, in both complete and CSS media, knockdown of ACTN4 significantly decreased the proliferation of LNCaP-AI cells.
ACTN4 regulates trophoblast invasion and migration. It regulates the AKT and GSK3b pathways. Therefore, its absence in PE can result in an underdeveloped embryo. ACTN4-positive embryos have the highest percentage of PE cells. However, ACTN4-positive embryos have a high rate of spontaneous abortion.
ACTN4 is an important regulator of the AKT pathway and is expressed in CTBs and syncytiotrophoblasts of the first trimester. Downregulation of ACTN4 decreases the phosphorylation of AKT at Ser473 and its downstream effector GSK3b. ACTN4 knockdown inhibits the proliferation of villous trophoblasts and iEVTs, which may contribute to preeclampsia pathogenesis.
In the ELISA, a-ACTN4 antibody, HSPA5 antibody, and ACTB antibody are used. After incubation with these peptides, serum was collected at different time points and evaluated for reactivity. Serum samples were analyzed at different times from the start of pregnancy to day 18. Results were summarized by the horizontal line, which represents the meanC2S.D. of the control absorbance. Sera containing antibodies that were detected in the samples had an OD greater than or equal to this line.
Samples were fixed with 4 % paraformaldehyde and permeabilized with 0.2 % Triton X-100. Secondary antibodies were then added to the samples and incubated for 30 min at room temperature. Finally, a DAB solution was applied to visualize the bands and sections were counter-stained with haematoxylin. These experiments are supported by the Nanjing JianCheng Bioengineering Institute.
To test whether the ACTN4 antibody works, it was used in immunohistochemistry to evaluate specificity of the antipeptide antibodies. The peptides HSPA5, ACTB, and a-ACTN4 were used as targets. Control animals did not react with the peptides. In this study, antisera used in immunohistochemistry were tested on mouse whole ovarian lysate. The pooled antisera recognized both oocytes and theca.
In addition to the ACTN4 anti-human T-cells, Boster Bio primary antibodies using the ACTG4 marker showed positive results in mice immunized with PBS. After obtaining images of the ACTN4-positive T-cells, we performed immunocytochemistry using previously published methods. The corresponding antibodies are listed in Supplement Table 3.
In addition to ACTN4, the Boster Bio primary antibody against this marker also binds to GSK3b. It is a crucial component of trophoblast migration and invasion. It may contribute to poor placentation and PE. The primary antibodies against ACTN4 have been used in a number of studies. If you are interested in using this antibody in your research, contact Boster Bio today.
The ACTN4 gene is a tumor suppressor, with the corresponding RNA profile exhibiting a difference. RNA profiles were consistent across gene sets (88%) and the ACTN4 gene exhibited a different profile. The ACTN4 interactome also displayed some disruptions, including dysregulation of LIM domain proteins, which are important modular regulators of cell adhesion.
In human podocytes, ACTN4 proteins with disease-causing mutations aggregate with F-actin. This mutation uncovered a previously buried actin-binding site, which increased the protein's actin-binding affinity and abolished Ca(2+) regulation. Mutant ACTN4 mislocalized focal adhesions and actin stress fibers, altering their biomechanical properties.
The ACTN4 marker has recently been studied in the context of cancer therapy. This new biomarker is highly expressed in bladder cancer cells and can improve the prognosis of patients with this disease. It has been shown to suppress cell proliferation and promote invasion. These properties may explain the association between high ACTN4 expression and bladder cancer prognosis. However, further study is needed to determine its exact role in the treatment of bladder cancer.
ACTN4 is a member of the a-actinin family and is involved in cytoskeletal reorganization. Human ACTN isoforms consisting of ACTN1, ACTN2, ACTN3, and ACTN4. ACTN1 is found at the interface of actin stress fibers, whereas PTCN4 appears to cross-link actin filaments. It is highly abundant in the leading edge of motile cells and cytoplasmic regions containing sharp cell extensions.
In cancer research, ACTN4 is preferentially expressed in moving structures, such as blood vessels, tumors, and nerves. ACTN4 is also associated with metastasis and invasion of cancer cells. Breast and non-small cell lung cancer patients with high ACTN4 expression had a worse prognosis than those with low expression. Furthermore, overexpression of ACTN4 in colon cancer cells was associated with lymph node metastasis in an animal model. Finally, ACTN4 has been associated with bladder cancer invasion and metastasis in a number of different tumor types.
ACTN4 CNI has been associated with poorer outcomes in patients with HR-positive, HER2-negative, node-negative breast cancer. In a study involving 261 patients, ACTN4 suppression reduced the invading tumor cells while increasing the phosphorylation of Akt, STAT3, and ERK. This finding suggests that the ERK pathway may play a role in the increased proliferation of bladder cancer cells.
Despite the lack of conclusive evidence regarding genetic modifiers of human ACTN4-mediated kidney disease, mice carrying the heterozygous ACTN4 mutant allele were found to have gradual glomerular filtration rate (KVD). In contrast, in humans, the early onset of kidney damage is more severe and progressive than in mice with homozygous Actn4 mutations.
PMID: 10656685 by Nikolopoulos S.N., et al. The human non-muscle alpha-actinin protein encoded by the ACTN4 gene suppresses tumorigenicity of human neuroblastoma cells.
PMID: 22567897 by Aksenova V.I.U., et al. Novel splicing isoform of actin-binding protein alpha-actinin 4 in epidermoid carcinoma cells A431.
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