ZFP36L2 Antibodies

mRNA decay activator protein ZFP36L2 (ZFP36L2)

Zinc-finger RNA-binding protein that destabilizes several cytoplasmic AU-rich element (ARE)-containing mRNA transcripts by boosting their poly(A) tail removal or deadenylation, and hence provide a mechanism for attenuating protein synthesis (PubMed:25106868, PubMed:14981510). Acts as a 3'-untranslated region (UTR) ARE mRNA-binding adapter protein to convey signaling events to the mRNA decay machinery (PubMed:25106868).

Functions by recruiting the CCR4-NOT deadenylase complex and probably other components of the cytoplasmic RNA decay machinery to the bound ARE-containing mRNAs, and hence promotes ARE-mediated mRNA deadenylation and decay processes (PubMed:25106868). Promotes ARE- containing mRNA decay of this low-density lipoprotein (LDL) receptor (LDLR) mRNA in response to phorbol 12-myristate 13- acetate (PMA) treatment in a p38 MAPK-dependent manner (PubMed:25106868).

Gene Information

Human
Gene Name:	ZFP36L2
Uniprot:	P47974
Entrez:	678

Family

Belongs to:
No superfamily

Alternative Names

HF.10; HF10Zinc finger protein HF.10; Zfp105; zinc finger protein 35 (clone HF.10); zinc finger protein 35

Molecular Weight

Mass (kDA):
51.063 kDA

Genomic Context

Human
Location:	2p21
Sequence:	2; NC_000002.12 (43222402..43226606, complement)

Tissue Specificity

Expressed mainly in the basal epidermal layer, weakly in the suprabasal epidermal layers (PubMed:27182009). Expressed in epidermal keratinocytes (at protein level) (PubMed:27182009).

Subcellular Localizations

Nucleus. Cytoplasm. Shuttles between the nucleus and the cytoplasm in a XPO1/CRM1-dependent manner.

Diseases

• Inflammation
• Infertility
• Female Infertility
• Leukemia
• Leukemia, Myelocytic, Acute
• Neoplasms
• Myeloid Leukemia
• Monosomy
• Burkitt Lymphoma
• Adult Acute Myeloblastic Leukemia
• Flt3 Internal Tandem Duplication
• Pancytopenia

• Insulin Resistance
• Dysplasia
• Chromosome 14 Trisomy Syndrome
• Malignant Neoplasms
• Hemorrhage
• Lymphoma
• Chimera Disorder

Pathways

• Localization
• S Phase
• Cell Migration
• Cell Proliferation
• Regulation Of Macrophage Activation
• Regulation Of Gene Expression
• Nuclear Export
• Macrophage Activation
• Response To Oxidative Stress
• Sensitization
• Translation

• Cell Motility
• Cell Cycle
• Cellular Localization
• Mrna Stabilization
• Wound Healing
• Pathogenesis

PTMs

• Phosphorylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ZFP36L2

Best Uses Of The ZFP36L2 Marker

The ZFP36L2 mark is a highly-specific, versatile tool. It can monitor the expression a variety Treg-associated molecular markers in different tissues and cells. This marker is not always useful, however, and it can give false positives. To make the process even more precise, you should conduct several tests to confirm that the ZFP36L2 markers are active.

ZFP36L2

The ZFP36L2 gene is a marker that inhibits Helios and other Treg associated molecules in T cells. This gene has been linked in some cases to autoimmune diseases like MS and SLE. SLE patients had lower levels of this gene. The protein was also identified as a susceptibility gene for MS in patients with SLE. Researchers identified ZFP36L2 from this study as a biomarker to these diseases.

This gene is expressed on human T cells CD4+. The study showed that ZFP36L2 reduces the function and stability of Ikzf2 mRNA. Thus, selective fine-tuning of this gene can help treat autoimmune diseases. Gene Expression Omnibus (GEO), GSE150937 has the datasets used. The Institutional Review Board from Chiba University reviewed the experiments.

The use of ZFP36L2 in colitis models was explored. In RAG2-/ mice, the gene product was co-injected in combination with naive CD4+T cells. Colitis was evaluated using histological analysis and weight measurements. The mice without ZFP36L2 had colitis. Mice with mock-injected ZFP36L2 had higher luciferase activity. This suggested the marker may be useful for treating colitis.

The ZFP36L2 gene product has great relevance for immunological research. It blocks the suppression of iTregs during various cancers. It is also useful in HIV Research, where it can identify disease-associated cells. It is a great tool both for clinicians and researchers. This gene product can also be used to characterize immune cells in your lungs.

Ikzf2

The best use for the ZFP36L2 marker in cancer diagnosis is This gene is very abundant in cancer cells. It is important to determine if it is present in the cancer. The ZFP36L2 gene is also expressed in other cells, such as the glioma, as it helps in the identification of cancer stem cells. Although the gene is expressed in glioma cell cells, it is not found in normal human cells. This gene's expression depends on the cancer cell's state, so a genetically valid model is needed to detect it.

Boster Bio ZFP36L2 genes are important markers for cancer research. It is found within the cells of HEK293 cells and corresponds a complex number of proteins. However, ZFP36L2 is not often found in the human body. The best use of this gene is dependent on its sensitivity. The Boster ZFP36L2 gene marker is compatible with all other genes, including MIG and MIN.

Boster Bio ZFP36L2 was expressed in naive, CD4+ T cells and rapidly decreased upon stimulation with T cell receptors. Its expression in regulatory T cells is lower than that of effector T cells. It inhibits Foxp3+ and Helios growth. It binds directly with the 3' untranslated region of Ikzf2 mRNA to destabilize its AU rich elements.

Helios

The recent discovery of the ZFP36L2 gene that inhibits Helios expression in iTregs suggests that this protein is necessary for Treg function. Helios expression could be controlled by many mechanisms. Future studies will need to determine which ones are most important. Although it is not clear what ZFP36L2 does to regulate Helios, the study suggests that it could help improve our understanding of how iTregs function in the immune system.

Naive CD4+T cell lines were used to investigate the ability ZFP36L2 has to regulate Helios transcription. They were stimulated with an Anti-CD3/Anti-CD28 mAb for 24 hours and then infected using MSCV-IRES–hNGFR(MIN)-Zfp36. After 48 hours of incubation cells were stained for Helios using flow cytometry analysis.

It was shown that the Helios marker was associated with both responding and nonresponse samples. This study raises the possibility that a significant percentage of thymic-derived Treg cells may be generated extrathymically. Although the marker did not identify the cells that responded to T cell treatment, it showed the differential role of Helios and ICOS in regulating T-cell function.

Using immunohistochemistry, the researchers have shown that ZFP36L2 expression inversely correlates with Helios expression in Tregs. When CD4+ Helios+ and CD4+ YFP+ were compared, the results were identical. These data were derived from two independent experiments. The paper provides more information about ZFP36L2's role in T-cell function regulation.

Other Treg-associated molecules

Numerous studies have shown other Treg-associated molecule are responsible to immune homeostasis. It is a crucial premise for preventing autoimmune diseases. Specifically, they influence the expression of Foxp3 and sPLA2-IID, two proteins secreted by Treg cells. In vitro studies have shown that both these molecules are essential for Treg differentiation. This may explain why they are possible therapeutic targets for many autoimmune and inflammatory disorders.

Researchers have discovered molecules that inhibit T cell activity in order to better understand Treg-mediated immune responses. These soluble compounds include IL-10 (TGF-b). In vitro experiments have shown that Treg cell responses to ubiquitous soluble proteins are strong. Tregs can recognize a number autoantigens and persistent pathogens. Further studies will reveal which of these antigens Tregs recognize.

Natural Tregs, which are CD4+CD25+Foxp3+cells, play an important role for immunologic self tolerance. Foxp3 regulates inflammatory, autoimmune and other responses. TGFb and IL-2 receptors are also Treg-associated molecules. Although the mechanisms of Treg immune regulation are not well understood, they contribute to Treg cells' stability in inhibiting activity. In vitro studies demonstrate that Helios+ Tregs have a higher suppressive capacity than their Foxp3 deficient counterparts. Additionally, mice lacking Helios+ Tregs are more susceptible to developing autoimmune disease after five and six month. Helios-deficient Tgs also reduce Foxp3 and upregulate inflammation cytokines.

The appearance of Heliosmid cell in the body coincides with the death of FOXP3 from Treg cells. This suggests Helios is more reliable for T cell growth than FOXP3. These molecules could be more useful for Treg-associated molecules than FOXP3 if they can be identified in their exact locations. The study will also reveal the location of other molecules that are essential for Tregs to function properly.

Assays for RNA Electrophoretic Mobility Shift

RNA electrophoretic molecular shift assay (EMSA), a technique that detects protein-nucleic Acid interactions, is a good choice. This technique detects the movement of protein-nucleic complexes, which is much slower than that of the unattached nucleic acid. These assays have many advantages, including the possibility to detect single-strandedDNAs and the ability of accommodating a wide range in nucleic acid sizes.

EMSAs may be performed with complex mixtures (or cell extracts) of proteins. EMSAs are able to reveal a wide range RNA-protein interactions. They can be performed with simple protein-binding events or complex formation and assembly RNA-protein complexes. EMSAs can be used to study the role mRNA has in various processes from gene expression to cancer research.

Zfp36L2 is a conserved protein in vertebrates. However, it is not known which mRNA targets it targets. Additionally, Zfp36l2-RNA compounds were not disrupted when antibodies bound to the carboxyl terminus Zfp36l2 are present. These antibodies were not also disrupted by amino acid. These antibodies were not disrupted by amino acids. RNA electrophoretic mobility shifting assays using ZFP36L2 markers may be a great tool in identifying genes that produce a specific protein.

Gel-purification can be used to purify RNA by using the ZFP36L2 markers. After purification, the RNA will form a single band on the gel. During this process, labeled RNA must be in appropriate binding conditions. These include 20 UL of Binding fluid, 1 UL of RNA, up to 4 UL of protein orRNA.

Application in iTregs

The role of iTregs in the development of autoimmune diseases is still unclear, but the development of polyclonal iTregmtDCs has demonstrated their potential as therapeutic agents in the field of autoimmune diseases. These iTreg cells may also serve as novel immunotherapy agents for the treatment of autoimmune diseases. The role of mtDCs is also important in the induction/expansion of iTregs.

These studies proved that iTregmtDC boosted iTregs while maintaining their regulatory phenotypes. To determine the impact of iTregmtDC upon the development of CIA in mice, clinical scores and the incidence rate of inflammatory arthritis were used. iTregs could also be beneficial in the treatment of other inflammatory conditions. Further, iTregmtDC has been shown to be able to promote the growth mtDC-containing immuno cells in human tissues.

Although tTregs may be more effective at suppressing disease related inflammation, they still display poorer differentiation. The iTregs that survive in the absence of Trp have a greater aerobic activity and a higher respiration rate than those that are raised in a Teff culture. The data shown represent three independent experiments and indicate greater potential for human immunotherapy. This therapy could be the best for immunotherapy of autoimmune diseases.