#STAT6 Antibody

[bostorbio]

STAT6 Antibody  - Boster Bio

Polyclonal antibodies are produced when mice are immunised with a synthetic peptide that mimics Stat6 (STAT6 Antibody) residues around amino acid 620. Research in immunology use protein A and peptide affinity chromatography to separate antibodies from antigens.

An interleukin 4 and an interleukin 13-induced signalling cascade include the Janus family of tyrosine kinases (Jak) and the STAT signal transduction pathway, which includes the inflammatory cytokine receptor 6 (STAT6) (1). There has been some evidence that STAT6 (predicted molecular weight 94kDa) may be responsible for the cytokine's anti-apoptotic properties. To activate transcription, the STAT family members gather in the nucleus once they have been phosphorylated by the receptor associated kinases.

This activation occurs when STAT6 is phosphorylated (Tyr641) in response to cellular interaction with IL-4.This gene has been located in the lymphocytes of the periphery as well as in the colon and the intestinal tract and in the ovaries as well as in the prostate as well as in the thymus and spleen. An crucial function for STAT6 in Th2 and Th9 responses is played by this transcription factor (2). When STAT6 (STAT6 Antibody) is deficient in mice, IL-4-mediated activities such as Th2 helper T cell generation, production of cell surface markers, T-cell proliferation, immunoglobulin class flipping to IgE, and a partial loss of IL-4-mediated proliferation are all affected. Allergies to nuts and malignant hemangiopericytomas have a link with the overexpression of STAT6.

[skinnijene-blog]

How a small molecule can defeat asthma attacks

Current treatments try to relieve so patients can breathe easily. Procedures might also include steroids to close down the inflammation that scientists have an idea for many decades underlies airway constriction. Inflammation of the airway ends in shortness of breath, and that may make humans panic and head to the emergency room. Corry's laboratory has been analyzing allergies for about 20 years. One of their pastimes is to understand better the molecular pathways that force airway constriction.

The makings of an allergies attack

An allergies attack is whatever but a natural event. It begins while environmental elements -- allergens -- enter the lungs and spark off a chain response of molecular pathways that spark off the development of the disease. Allergens spark off immune cells, recruiting them to the lungs and leading a number of them to provide a robust IgE antibody reaction and others to secrete immune mediators called cytokines. Cytokines IL-four and IL-13 especially are required for asthma to manifest. These cytokines spark off every other molecule, transcription component STAT6, that drives the expression of some genes, in the end, leading to the exaggerated contraction of the airlines that causes the tons feared shortness of breath.

Mice which can be genetically engineered to lack STAT6, also lack the responses induced with the aid of the IL-4/IL-thirteen/STAT6 interplay and are resistant to bronchial asthma attacks.

"STAT6 is at the epicenter of the immune responses that mediate asthma, so we looked for a way to block STAT6 activation," stated Dr. J. Morgan Knight, post-doctoral fellow inside the Corry lab. "To prompt STAT6, IL-4 and IL-13 bind to their corresponding receptors on immune cells. These receptors percentage a critical subunit known as IL4R-alpha that activates STAT6. However, additional studies from our lab have shown that special receptors can also spark off STAT6. So, we centered our efforts on developing a small-molecule that could bind to and inhibit STAT6 activity without delay."

David defeats Goliath

Such efforts are not any small feat. Corry, Knight and their colleagues had to design a small molecule able to especially targeting STAT6, that's in the cells of the lungs, without also triggering unwanted side outcomes.

"After years of work, we succeeded," said Knight. "We chemically synthesized a small molecule called PM-43I which could inhibit STAT6-based allergic airway disease in mice. Moreover, PM-43I reversed preexisting allergic airway sickness in mice with a minimum dose of 0.25? G/kg. Importantly, PM-43I changed into correctly cleared through the kidneys and had no long-term toxicity. We concluded that PM-43I represents the first of a class of small molecules that may be suitable for similarly medical improvement as a therapeutic drug in opposition to asthma."

[tumimmtxpapers]

Deceleration of glycometabolism impedes IgG-producing B cell-mediated tumor elimination by targeting SATB1.

Related Articles Deceleration of glycometabolism impedes IgG-producing B cell-mediated tumor elimination by targeting SATB1. Immunology. 2018 Sep 01;: Authors: Liu J, Li Y, Lu Z, Gu J, Liang Y, Huang E, Wang Z, Zhang H, Wang L, Zhang D, Yu H, Liu R, Chu Y Abstract B lymphocytes, known as antibody producers, mediate tumor-cell destruction in the manner of antibody-dependent cell-mediated cytotoxicity; however, their anti-tumor function seems to be weakened during tumorigenesis; while, the mechanisms underlying remained unclear. In this study, we found that IgG mediated anti-tumor effect, but IgG-producing B cells decreased in various tumors. Considering the mechanism underlying, glycometabolism was noteworthy. We found that tumor-infiltrating B cells were glucose-starved and accompanied by a deceleration of glycometabolism. Both inhibition of glycometabolism and deprivation of glucose through tumor cells, or glucose-free treatment reduced the differentiation of B cells into IgG-producing cells. In this process, special AT-rich sequence-binding protein-1 (SATB1) was significantly silenced in B cells. Downregulating SATB1 by Inhibiting glycometabolism or RNA-interference reduced the binding of STAT6 to the promoter of germline Cγ gene, subsequently resulting in fewer B cells producing IgG. Our findings provide the first evidence that glycometabolic inhibition by tumorigenesis suppress differentiation of B cells into IgG-producing cells, and altering glycometabolism may be of promising in improving anti-tumor effect of B cells. This article is protected by copyright. All rights reserved. PMID: 30171602 [PubMed - as supplied by publisher] http://dlvr.it/QhsBCF

[cancersfakianakis1]

Blocking IL4- and IL13-mediated phosphorylation of STAT6 (Tyr641) decreases M2 polarization of macrophages and protects against macrophage-mediated radioresistance of inflammatory breast cancer

Publication date: Available online 7 December 2017 Source:International Journal of Radiation Oncology*Biology*Physics Author(s): Omar M. Rahal, Adam R. Wolfe, Pijus K. Mandal, Richard Larson, Sanda Tin, Cristina Jimenez, Dadong Zhang, Janet Horton, James M. Reuben, John S. McMurray, Wendy A. Woodward PurposeThe purpose of this study was to determine the role of macrophage polarization on the response of IBC cells to radiation and whether modulation of macrophage plasticity can alter radiation response.Methods and MaterialsThe human THP-1 monocyte cell line and primary human monocytes isolated from peripheral blood mononuclear cells were differentiated into macrophages and polarized to either an “anti-tumor” (M1) or a “pro-tumor” (M2) phenotype. These polarized macrophages were co-cultured with IBC cells (SUM149, KPL4, MDA-IBC3, or SUM190) without direct contact for 24 h, then subjected to irradiation (0, 2, 4, or 6 Gy). Interleukin (IL)4/IL13-induced activation of STAT6 signaling was measured by Western blotting of phospho-STAT6 (Tyr641), and expression of M2 polarization gene markers (CD206, fibronectin, and CCL22) was measured by qPCR.ResultsExpression of M2 polarization markers was higher in M2-polarized macrophages after IL4/IL13 treatment than in control (M0) or M1-polarized macrophages. Co-culture of IBC cell lines with M1-polarized THP-1 macrophages mediated radiosensitivity of IBC cells, while co-culture with M2-polarized macrophages mediated radioresistance. Phosphopeptide mimetic PM37, targeting the SH2 domain of STAT6, prevented and reversed IL4/IL13-mediated STAT6 phosphorylation (Tyr641) and decreased the expression of M2 polarization markers. Pretreatment of M2-THP1 macrophages with PM37 reduced the radioresistance they induced in IBC cells after co-culture. Targeted proteomics analysis of IBC KPL4 cells using a kinase antibody array revealed induction of PRKCZ in these cells only after co-culture with M2-THP1 macrophages, which was prevented by PM37 pretreatment. KPL4 cells with stable shRNA knockdown of PRKCZ exhibited lower radioresistance after M2-THP1 co-culture.ConclusionsThese data suggest that inhibition of M2 polarization of macrophages by PM37 can prevent radioresistance of IBC by downregulating PRKCZ.

Teaser

Here we show that M2-polarized macrophages upon co-culture with IBC cells, promote radioresistance of IBC cells, and this effect was inhibited by PM37, a phosho-STAT6 inhibitor. M2-macrophages mediated radioresistance of KPL4 IBC cells is associated with increased protein expression of PRKCZ kinase in KPL4 cells, after M2-macrophage co-culture, and this was prevented by PM37-mediated inhibition of M2 polarization of THP1 macrophages prior to coculture with KPL4 cells. http://ift.tt/2B0c6DV

[antibodyproductsservice5]

Purchase The Best-Produced Limk2 Product From Capralogics

Various medical researchers nowadays focus on manufacturing the best antibodies that can cure severe diseases. They are the vaccination used to reduce the transmission of infection, associated with the use of human plasma driven products. Several custom antibodies are getting developed these days through preparing antigens with the help of animals like goat, sheep, chicken, guinea pig, horses and more. These animals are frequently used to create the polyclonal products, which help humans in recovering from harmful infectious diseases. If you are looking for a full-service antibody production facility provider for your pharmaceutical industry, you should get in touch with Capralogics Inc. Our experts have professional expertise in creating medicines like LIMK2, which is really helpful in curing cardiovascular disorders.

Along with the LIMK product, we also have a different range of products like anti-STAT6, DCK, FADK, Goat Anti –Alpaca IgG, sheep anti-histone III and more. We are striving to become one of the best service providers in our industry and focus on providing the best quality items to the entire pharmaceutical industry. With our expertise, we assure that we are going to be a trustworthy partner, who can implement a custom solution as per your requirement. Our professionals are knowledgeable enough to propose a tailored process to create the best solution for people to get an effective treatment to cure bacterial infections. We have already assisted several clients and are currently working as a reliable partner with various companies. So, if you have any query regarding our services or looking for our products, feel free to contact us.To more information visit our website www.capralogics.com

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[bostorbio]

Boster Bio Anti-STAT6 Antibody Picoband™ catalog # PB9405. Tested in WB applications. This antibody (STAT6 antibody) reacts with Human, Rat.

[antibodyproductsservice5]

Purchase The Best-Produced Limk2 Product From Capralogics

Various medical researchers nowadays focus on manufacturing the best antibodies that can cure severe diseases. They are the vaccination used to reduce the transmission of infection, associated with the use of human plasma driven products. Several custom antibodies are getting developed these days through preparing antigens with the help of animals like goat, sheep, chicken, guinea pig, horses and more. These animals are frequently used to create the polyclonal products, which help humans in recovering from harmful infectious diseases. If you are looking for a full-service antibody production facility provider for your pharmaceutical industry, you should get in touch with Capralogics Inc. Our experts have professional expertise in creating medicines like LIMK2, which is really helpful in curing cardiovascular disorders.

Along with the LIMK product, we also have a different range of products like anti-STAT6, DCK, FADK, Goat Anti –Alpaca IgG, sheep anti-histone III and more. We are striving to become one of the best service providers in our industry and focus on providing the best quality items to the entire pharmaceutical industry. With our expertise, we assure that we are going to be a trustworthy partner, who can implement a custom solution as per your requirement. Our professionals are knowledgeable enough to propose a tailored process to create the best solution for people to get an effective treatment to cure bacterial infections. We have already assisted several clients and are currently working as a reliable partner with various companies. So, if you have any query regarding our services or looking for our products, feel free to contact us.To more information visit our website www.capralogics.com

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[cancersfakianakis1]

FNA cytology of solitary fibrous tumors and the diagnostic value of STAT6 immunocytochemistry

BACKGROUND

Solitary fibrous tumors (SFTs) are rare mesenchymal tumors commonly located in the pleura, soft tissues, or meninges and are characterized by the NGFI-A-binding protein 2 (NAB2)–signal transducer and activator of transcription 6 (STAT6) fusion gene. Recent studies have indicated that nuclear STAT6 immunohistochemistry is a specific marker for SFTs.

METHODS

The authors reviewed fine-needle aspiration (FNA) specimens from extracranial SFTs diagnosed at their institution between 1993 and 2017. Histologic blocks and available formalin-fixed smears of FNA specimens from SFTs were investigated for STAT6 immunoreactivity using a monoclonal antibody. STAT6 immunocytochemistry was also investigated in schwannomas and spindle cell lipomas. Cytopathologic and clinical characteristics were described.

RESULTS

Nineteen benign and 9 malignant SFTs were identified. Both benign and malignant SFTs had a female predominance (female-to-male ratio, 2.8:1 and 1.25, respectively). Localization varied, and approximately one-half of the extrapleural tumors were located in the extremities and frequently were intramuscular. Benign and malignant primary tumors had limited differences in cytologic presentation, the most notable feature being nuclear pleomorphism. Cytomorphologic features included low-to-moderate cellularity of mixed oval, elongated, round, and stellate cells with pink collagenous stroma and hypercellular clusters with infrequent atypia. In metastatic SFTs, the cytopathology was suggestive of sarcoma. Immunohistochemistry revealed nuclear STAT6 immunoreactivity in SFTs (n = 5) with cytoplasmic reactivity in cytologic mimickers.

CONCLUSIONS

Benign and malignant SFTs have common cytopathologic features, and the ability to distinguish between them is limited. Nuclear STAT6 immunoreactivity is a valuable cytologic marker for SFTs. Cancer Cytopathol 2017. © 2017 American Cancer Society.

http://ift.tt/2jw6VUP

[cancersfakianakis1]

Soft tissue angiofibroma – clinicopathologic, immunohistochemical and molecular analysis of 14 cases

Abstract

Soft tissue angiofibroma is rare and has characteristic histomorphological and genetic features. For diagnostic purposes, there are no specific antibodies available. Fourteen lesions (6 females, 8 males; age range 7 - 67 years) of the lower extremities (12) and trunk (2) were investigated by immunohistochemistry, including for the first time NCOA2. NCOA2 was also tested in a control group of other spindle cell lesions. The known fusion-genes (AHRR-NCOA2 and GTF2I-NCOA2) were examined using RT-PCR in order to evaluate their diagnostic value. Cases in which no fusion gene was detected were additionally analysed by RNA sequencing. All cases tested showed nuclear expression of NCOA2. However, this was not specific since other spindle cell neoplasms also expressed this marker in a high percentage of cases. Other variably positive markers were EMA, SMA, desmin and CD34. STAT6 was negative in the cases tested. By RT-PCR for the most frequently observed fusions, an AHRR-NCOA2 fusion transcript was found in 9/14 cases. GTF2I-NCOA2 was not detected in the remaining cases (n = 3). RNA sequencing revealed three additional positive cases; two harbored a AHRR-NCOA2 fusion and one case a novel GAB1-ABL1 fusion. Two cases failed molecular analysis due to poor RNA quality. In conclusion, the AHRR-NCOA2 fusion is a frequent finding in soft tissue angiofibroma, while GTF2I-NCOA2 seems to be a rare genetic event. For the first time, we report a GAB1-ABL1 fusion in a soft tissue angiofibroma of a child. Nuclear expression of NCOA2 is not discriminating when compared with other spindle cell neoplasms. This article is protected by copyright. All rights reserved.

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