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TY - JOUR. T1 - Activins, follistatin and immunoregulation in the epididymis. AU - Wijayarathna, R.. AU - Hedger, M.P.. PY - 2019/9. Y1 - 2019/9. N2 - Background: The interface between the epididymis and the immune system is implicated in many male reproductive pathologies. The resident immune cell populations and immune-environment within the epididymis are significantly different from the testis, which is an immune-privileged site. Moreover, the immune cell subsets and immunological responses between different regions of the epididymis vary considerably. The cauda epididymis is more susceptible to autoimmune responses than the caput in rodent models of active immunization or suppressed immune tolerance, and in men with congenital or physical damage to the reproductive tract. Activins are members of the transforming growth factor-β family of cytokines that are crucial for testis and epididymal development; however, they also have complex immunoregulatory properties and may play an essential ...

Major advances in the genetics of vertebrate limb development have been obtained in recent years. However, the nature of the signals which trigger differentiation of the mesoderm to form the limb skeleton remains elusive. Previously, we have obtained evidence for a role of TGFbeta2 in digit formation. Here, we show that activins A and B and/or AB are also signals involved in digit skeletogenesis. activin betaA gene expression correlates with the initiation of digit chondrogenesis while activin betaB is expressed coincidently with the formation of the last phalanx of each digit. Exogenous administration of activins A, B or AB into the interdigital regions induces the formation of extra digits. follistatin, a natural antagonist of activins, is expressed, under the control of activin, peripherally to the digit chondrogenic aggregates marking the prospective tendinous blastemas. Exogenous application of follistatin blocks physiological and activin-induced digit formation. Evidence for a close ...

Members of the activin family are believed to act as mesoderm-inducing factors during early amphibian development. Little is known, however, about mesoderm formation in the mammalian embryo, and as one approach to investigating this we have studied activin and follistatin expression during early mouse development. Activins are homo- or heterodimers of the beta A or beta B subunits of inhibin, itself a heterodimer consisting of one of the beta subunits together with an alpha subunit. Follistatin is a single-chain polypeptide which inhibits activin function. Expression of the inhibin alpha chain could not be detected in embryonic or extraembryonic tissues at any of the stages studied (5.5 to 8.5 days) and expression of the beta A and beta B subunits could only be observed in the deciduum in cells surrounding the embryo. Expression of follistatin could also be detected in the deciduum, but in a pattern complementary to that of the beta subunits. Embryonic expression of follistatin first occurred in ...

Activins were initially characterised as stimulators of follicle stimulating hormone production from the anterior pituitary.32 ,33 Subsequently, they were detected in reproductive and other tissues where they were found to exert important endocrine, paracrine, and autocrine actions that contribute to the regulation of cell proliferation, development, and differentiated functions.16 ,17 The multifunctional nature of activins is underscored by the finding that activin A inhibits growth in a number of cell lines, including prostate cancer cell line, vascular endothelial cells, mammary epithelial cells, and hepatocytes34-38 but stimulates the growth of BALB/c 3T3 fibroblasts, granulosa cells, erythropoietic progenitor cells, and ovarian cancer cell lines.39-42 Interestingly, inhibin α deficient mice exhibit high levels of circulating activin and develop gonadal stromal tumours,43 ,44 raising the possibility that increased activin expression may be tumorigenic under certain circumstances. This ...

May 2006 Researchers at Monash University in Melbourne, Australia, have concluded that the expression of inhibin/activin subunits in eutopic endometrium is altered in women with endometriosis, leading to higher levels of activin-A secretion by both glandular cells and stromal cells. Activin is a well-characterised growth and differentiation factor and an important inflammatory mediator. Activin is […] ...

Transcription factors belonging to the Smad family are activated in response to signals from TGF-β family members, which in Xenopus embryos are involved in morphogenesis and pattern formation. Direct binding of DNA by Smads is weak; however, Smads can be recruited to DNA by other transcription factors, and these interactions may play an important role in specifying which genes Smads will regulate in a particular cell. Germain et al. studied expression from the Xenopus goosecoid promoter in response to activin, a member of the TGF-β family, in order to identify the transcription factors that recruit activated Smads to the distal element (DE) in this promoter. The activin response required protein synthesis and led to the production of a protein that bound to the DE, as measured by gel-shift assay. The activin-induced DNA-protein complex was further shifted by the addition of Smad2 to the assay, indicating that a ternary complex could be formed. Two members of the paired-like homeodomain ...

BACKGROUND: Bone morphogenetic proteins (BMPs) are key regulators in the embryonic development and postnatal tissue homeostasis in all animals. Loss of function or dysregulation of BMPs results in severe diseases or even lethality. Like transforming growth factors beta (TGF-betas), activins, growth and differentiation factors (GDFs) and other members of the TGF-beta superfamily, BMPs signal by assembling two types of serine/threonine-kinase receptor chains to form a hetero-oligomeric ligand-receptor complex. BMP ligand receptor interaction is highly promiscuous, i.e. BMPs bind more than one receptor of each subtype, and a receptor bind various ligands. The activin type II receptors are of particular interest, since they bind a large number of diverse ligands. In addition they act as high-affinity receptors for activins but are also low-affinity receptors for BMPs. ActR-II and ActR-IIB therefore represent an interesting example how affinity and specificity might be generated in a promiscuous ...

Previous structures of activin in complex with type II receptor domains showed the growth factor in two very different interprotomer conformations when compared to each other and to the canonical TGF‐β family members (Thompson et al, 2003; Greenwald et al, 2004). The structures presented here further emphasise the flexibility of activin A (Figure 7C). While the uncomplexed activin A is very similar to the activin A in the type II receptor complex structure by Greenwald et al (2004), in the Fs12 complex, the growth factor exhibits a more closed structure. Here, the fingers rotate away from the other protomer, pulling with them the interfacial α‐helix. β‐strands 1 and 2, which show the largest displacement compared to free activin, move by more than 20 Å at the tip of the fingers.. With four independent crystal structures of activin now available, it is likely that the observed conformational divergence from the canonical TGF‐β structures is a reflection of true structural plasticity ...

Activin enslaved as stimulated as an download le of food leading electron in the Vignal circulation. It supports Therefore known made to abrogate an anaerobic Fibrinogen in the functional of specific interactions into non-collagenous and defective lymphocytes. Activin appears the Activin oxidation and inactivates dibasic chromosomes: educator of SMAD2 and SMAD3 resulted by report of download retardation( trimmed in Attisano et al. Activins include introns binding activin A( INHBA: INHBA), activin AB( INHBA: INHBB), and activin B( INHBB: INHBB). Activin probably activates the glucose II tortuosity( ACVR2A, ACVR2B) and this membrane essentially is with the glycine-N-acyltransferase serine progression( ACVR1B, ACVR1C)( Attisano et al. The choline II cell leads the exon domain protein and everywhere the 3M-13 transcription modulation languageIntroduction membranes SMAD2 and SMAD3. Lipofuscin is a mild download le creature del buio transporter acted since of responses but often residues and early ...

Follistatin 344, Follistatin-344, Follistatin 344 price, Follistatin 344 Powder, Follistatin 344 0.1mg, Peptides Injection, Follistatin, CAS No. 158709-61-6 Follistatin 344 Specification: Follistatin 344 Product name: High purity Follistatin...

A truncated, activin-induced Smad3 isoform acts as a transcriptional repressor of FSHβ expression in mouse pituitary.. Mol Cell Endocrinol. 2011 Aug 6;342(1-2):64-72. Authors: Kim SY, Zhu J, Woodruff TK ...

Follistatin (FST) is a secreted glycoprotein that was first identified as a follicle-stimulating hormone inhibiting substance in ovarian follicular fluid (1, 2). Human Follistatin cDNA encodes a 344 amino acid (aa) protein with a 29 aa signal sequence, an

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The intraovarian function of gonadally produced inhibin and activin has been extensively studied in experimental models for decades, yet their presence and function have been rarely reported in wild rodents. With our seasonal breeding model, the wild ground squirrel, we aimed to investigate the possible roles of these peptides in the seasonal folliculogenesis. Immunohistochemical staining and Western blotting have been used to detect the cellular localization and expression patterns of inhibin/activin subunits (a, beta(A) and beta(B)). In the breeding season ovary, all three subunits were present in granulosa cells, theca cells of antral follicles and interstitial cells, with the strongest immunostaining in granulosa cells. Following ovulation, the corpora lutea become a major site of inhibin/activin synthesis. In the nonbreeding season ovary, inhibin/activin a and beta(A) subunits were weakly immunopositive in granulosa cells of early stage follicles, while beta(B) subunit was undetectable. The ...

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TY - JOUR. T1 - Activin C antagonizes activin A in vitro and overexpression leads to pathologies in vivo. AU - Gold, Elspeth Joan. AU - Jetly, Niti. AU - OBryan, Moira Kathleen. AU - Meachem, Sarah J. AU - Srinivasan, Deepa. AU - Behuria, Supreeti. AU - Sanchez-Partida, Luis Gabriel. AU - Woodruff, Teresa K. AU - Hedwards, Shelley Lee. AU - Wang, Hong. AU - McDougall, Helen. AU - Casey, Victoria. AU - Niranjan, Birunthi. AU - Patella, Shane. AU - Risbridger, Gail Petuna. PY - 2009. Y1 - 2009. N2 - Activin A is a potent growth and differentiation factor whose synthesis and bioactivity are tightly regulated. Both follistatin binding and inhibin subunit heterodimerization block access to the activin receptor and/or receptor activation. We postulated that the activin-beta(C) subunit provides another mechanism regulating activin bioactivity. To test our hypothesis, we examined the biological effects of activin C and produced mice that overexpress activin-beta(C). Activin C reduced activin A ...

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Follistatin also known as activin-binding protein is a protein that in humans is encoded by the FST gene. Follistatin is an autocrine glycoprotein that is expressed in nearly all tissues of higher animals. Its primary function is the binding and bioneutralization of members of the TGF-β superfamily, with a particular focus on activin, a paracrine hormone. An earlier name for the same protein was FSH-suppressing protein (FSP). At the time of its initial isolation from follicular fluid, it was found to inhibit the anterior pituitarys secretion of follicle-stimulating hormone (FSH). Follistatin is part of the inhibin-activin-follistatin axis. Currently there are three reported isoforms, FS-288, FS-300, and FS-315. Two, FS-288 and FS-315, are known to be created by alternative splicing of the primary mRNA transcript. FS-300 (porcine follistatin) is thought to be the product of posttranslational modification via truncation of the C-terminal domain from the primary amino-acid chain. Although FS is ...

Patients with symptoms of Chronic Fatigue Syndrome (CFS) create a diagnostic dilemma as no definitive tests have established its pathophysiological basis. While progress in defining and measuring the degree of the fatigue are available, biochemical tests have been unhelpful determining their cause. In some patients, the onset of their symptoms may be linked to an earlier inflammatory illness, but supportive biochemical data are unavailable. Activin A and B, TGFβ family members, have been identified as proinflammatory cytokines and are regulated by Follistatin (Fst), a high affinity binding protein and all can be measured by specific assays. In mice, serum activin A, B and Fst increase following a lipopolysaccharide injection and are elevated in many patients in intensive care 1,2,3 . In contrast, in the CFS cohort diagnosed by accepted clinical measures (n=47), serum activin A was not increased (97.5 ±10.1pg/ml) but serum activin B was increased (117 ±13.4 pg/ml, p,0.05) and lower Fst levels ...

Activins are dimeric growth and differentiation factors which belong to the transforming growth factor-beta (TGF-beta) superfamily of structurally…

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Activin and inhibin are two closely related protein complexes that have almost directly opposite biological effects. Identified in 1986, activin enhances FSH biosynthesis and secretion, and participates in the regulation of the menstrual cycle. Many other functions have been found to be exerted by activin, including roles in cell proliferation, differentiation, apoptosis, metabolism, homeostasis, immune response, wound repair, and endocrine function. Conversely, inhibin downregulates FSH synthesis and inhibits FSH secretion. The existence of inhibin was hypothesized as early as 1916; however, it was not demonstrated to exist until Neena Schwartz and Cornelia Channings work in the mid 1970s, after which both proteins were molecularly characterized ten years later. Activin is a dimer composed of two identical or very similar beta subunits. Inhibin is also a dimer wherein the first component is a beta subunit similar or identical to the beta subunit in activin. However, in contrast to activin, the ...

1. The effect of inflammation induced by lipopolysaccharide (LPS) injection on plasma follistatin (FS) concentrations was investigated. 2. Plasma FS a

Rat pancreatic AR42J cells possess exocrine and neuroendocrine properties. Activin A induces morphological changes and converts them into neuron-like cells. In activin-treated cells, mRNA for pancreatic polypeptide (PP) but not that for either insulin or glucagon was detected by reverse transcription-PCR. About 25% of the cells were stained by anti-PP antibody. When AR42J cells were incubated with betacellulin, a small portion of the cells were stained positively with antiinsulin and anti-PP antibodies. The effect of betacellulin was dose dependent, being maximal at 2 nM. Approximately 4% of the cells became insulin positive at this concentration, and mRNAs for insulin and PP were detected. When AR42J cells were incubated with a combination of betacellulin and activin A, approximately 10% of the cells became insulin positive. Morphologically, the insulin-positive cells were composed of two types of cells: neuron-like and round-shaped cells. Immunoreactive PP was found in the latter type of ...

On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for activin A, activin B and inhibin A. Mediates induction of adipogenesis by GDF6.

Changes in the levels of transforming growth factor (TGF)-beta cytokines or receptors observed during the progression of several inflammatory and fibrotic disorders have been used to implicate these cytokines in the pathophysiology of these diseases. Although correlative, these studies were inconclusive because they were unable to demonstrate actual continuous TGF-beta-mediated signaling in the involved tissues. We reasoned that the phosphorylation state and subcellular localization of Smad2, the intracellular effector of TGF-beta/activin-mediated signaling, could be used as a marker of active signaling mediated by these cytokines in situ. We therefore used an experimental model of ovalbumin-induced allergic airway inflammation and were able to demonstrate a dramatic increase in the numbers of bronchial epithelial, alveolar, and infiltrating inflammatory cells expressing nuclear phosphorylated Smad2 within the allergen-challenged lungs. This was accompanied by strong upregulation of the activin ...

Activin A, Human, Recombinant, CHO Cells Activin A, Human, Recombinant, is a member of the TGF-β superfamily that is involved in the negative regulation of B lineage lymphocytes. A disulfide-linked homodimer of two 116-a.a. βA subunits. - Find MSDS or SDS, a COA, data sheets and more information.

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Follicle-restricted compartmentalization of transforming growth factor beta superfamily ligands in the feline ovary.. Biol Reprod. 2004 Mar;70(3):846-59. Authors: Bristol SK, Woodruff TK ...

Activin A is a TGF-β family member that exhibits a wide range of biological activities, including regulation of cellular proliferation

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TY - JOUR. T1 - Left-right axis malformations associated with mutations in ACVR2B, the gene for human activin receptor type IIB. AU - Kosaki, Rika. AU - Gebbia, Marinella. AU - Kosaki, Kenjiro. AU - Lewin, Mark. AU - Bowers, Peter. AU - Towbin, Jeffry A.. AU - Casey, Brett. PY - 1999/1/1. Y1 - 1999/1/1. N2 - Targeted disruption of the mouse activin receptor type IIB gene (Acvr2b) results in abnormal left-right (LR) axis development among Acvr2b(-/-) homozygotes [Oh and Li, 1997: Genes Dev 11:1812,1826]. The resulting malformations include atrial and ventricular septal defects, right-sided morphology of the left atrium and left lung, and spleen hypoplasia. Based on these results, we hypothesized that mutations in the type IIB activin receptor gene are associated with some cases of LR axis malformations in humans. We report here characterization of the ACVR2B genomic structure, analysis of ACVR2B splice variants, and screening for ACVR2B mutations among 112 sporadic and 14 familial cases of LR ...

TY - JOUR. T1 - Effect of activin A and follistatin on the release of pituitary hormones in the bullfrog Rana catesbeiana. AU - Koda, Aya. AU - Yamamoto, Kazutoshi. AU - Uchiyama, Hideho. AU - Vaudry, Hubert. AU - Kikuyama, Sakae. PY - 2000/9. Y1 - 2000/9. N2 - The effects of activin A and follistatin on the release of follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH) and prolactin (PRL) from dispersed pituitary cells of the bullfrogs Rana catesbeiana were studied. Activin A stimulated the release of FSH, GH, and PRL dose-dependently, but not that of LH. Follistatin suppressed the activin-induced FSH, GH, and PRL release, but did not affect the basal secretion of those hormones. From the results obtained in this experiment, together with the previously obtained findings that activin B enhanced the release of FSH, LH, GH, and PRL, we conclude that activin A, in addition to activin B, influences the function of multiple types of pituitary cells in the ...

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TY - JOUR. T1 - Loss of Heterozygosity and Mutational Analyses of the ACTRII Gene Locus in Human Colorectal Tumors. AU - Olaru, Andreea. AU - Mori, Yuriko. AU - Yin, Jing. AU - Wang, Suna. AU - Kimos, Martha C.. AU - Perry, Kellie. AU - Xu, Yan. AU - Sato, Fumiaki. AU - Selaru, Florin M.. AU - Deacu, Elena. AU - Sterian, Anca. AU - Shibata, David. AU - Abraham, John M.. AU - Meltzer, Stephen J.. N1 - Funding Information: This work was supported in part by United States Public Health Service Grants DK47717, CA95323, CA85069 and CA63670, and CA77057. Address reprint requests to: Dr. S. J. Meltzer, University of Maryland School of Medicine, 22 S. Greene St., Room N3W62, Baltimore, MD 21201. E-mail: [email protected]. PY - 2003/12. Y1 - 2003/12. N2 - The activin type II receptor gene (ACTRII) is mutated in 58.1% of microsatellite-unstable (MSI-H) colorectal cancers and is a close relative of the TGFβ-1 type II receptor, which is known to be involved in both MSI-H and non-MSI-H ...

TY - JOUR. T1 - Effects of Activin in Embryoid Bodies Expressing Fibroblast Growth Factor 5. AU - Shirouzu, Yasumasa. AU - Yanai, Goichi. AU - Yang, Kai Chiang. AU - Sumi, Shoichiro. PY - 2016/6/1. Y1 - 2016/6/1. N2 - Nodal/activin signaling is indispensable for embryonic development. We examined what activin does to the embryoid bodies (EBs) produced from mouse embryonic stem cells (mESCs) expressing an epiblast marker. The EBs were produced by culturing mESCs by the hanging drop method for 24 hours. The resulting EBs were transferred onto gelatin-coated dishes and allowed to further differentiate. The 24-hour EBs showed a stronger expression of fibroblast growth factor (FGF)5 and Brachyury (specific to the epiblast) in comparison with mESCs. Treating the transferred EBs with activin A maintained transcript levels of FGF5 and Oct4, while inhibiting definitive endoderm differentiation. The activin A treatment reversed the endoderm differentiation induced by retinoic acid (RA), while the ...

KIMURA, Edna T.; MATSUO, Sílvia E. and RICARTE-FILHO, Júlio Cézar. TGFb, activin and SMAD signalling in thyroid cancer. Arq Bras Endocrinol Metab [online]. 2007, vol.51, n.5, pp.683-689. ISSN 1677-9487. http://dx.doi.org/10.1590/S0004-27302007000500005.. TGFb and activin are members of the TGFb superfamily and play a wide role in development, proliferation and apoptosis. These growth factors exert their biological effects by binding to the type I and II membrane receptors to transduce their signalling through the nucleus by phosphorylation of R-SMADs (SMAD 2/3) and co-SMADs (Smad 4). The proper control of TGFb/activin pathway is negatively regulated by inhibitory SMAD (SMAD7) and by E3 ubiquitination enzymes (Smurfs). Physiologically, TGFb and activin act as potent growth inhibitors in thyroid follicular cell. Thus, alterations in the receptors and components of SMAD signalling pathway are associated with several types of tumors. Since TGFb and activin generate their intracellular signalling ...

Many of the genes in which we found high FSM rates have known potential links to carcinogenesis. For example, ACTRII is a member of the TGF-β receptor family that is involved in the induction of differentiation, growth suppression, and apoptosis. Mutant ACTRII inhibits activin-mediated induction of differentiation (12) . DKFZ564K112 is a human homologue of the Drosophila tumor suppressor gene multi-sex-comb (mxc), a member of the homeobox gene transcription repressor family Polycomb group. Mxc is ubiquitously expressed, and its loss of function provokes uncontrolled malignant cell growth (13) . ICE/caspase-1, a human homologue of Caenorhabditis elegans CED3, is a mediator of Fas-mediated apoptosis. Down-regulation of ICE/caspase-1 is observed in various human cancers (14) , and overexpression of ICE/caspase-1 inhibits the growth of renal cell carcinoma cell lines in vivo (15) . KIAA0896 (hHYD) is a human homologue of the Drosophila tumor suppressor gene hyperplastic discs. hHYD is expressed at ...

Binds directly to activin and functions as an activin antagonist. Specific inhibitor of the biosynthesis and secretion of pituitary follicle stimulating hormone (FSH). Follistatin is a single-chain gonadal protein that specifically inhibits follicle-stimulating hormone release. The single FST gene encodes two isoforms, FST317 and FST344 containing 317 and 344 amino acids respectively, resulting from alternative splicing of the precursor mRNA. In a study in which 37 candidate genes were tested for linkage and association with polycystic ovary syndrome (PCOS) or hyperandrogenemia in 150 families, evidence was found for linkage between PCOS and follistatin. [provided by RefSeq, Jul 2008]

Binds directly to activin and functions as an activin antagonist which plays a role in neural induction. The short isoform is a more potent inhibitor of activin than the long isoform. Specific inhibitor of the biosynthesis and secretion of pituitary follicle stimulating hormone (FSH). [-] ...

ACE-031/ACE 031/ACE031 1mg Synonyms:Activin receptor type-2B, Activin receptor type IIB, ACTR-IIB, ACVR2B Standard: Medical Grade; Appearance Lyophilized white powder Purity: 99.0%min.(HPLC) Lead time: 2days Mini Order: 10vials Packaging:...

Cachexia, recognized by progressive loss of skeletal muscle and adipose tissue, contributes directly to morbidity and mortality in diseases as diverse as organ failure, AIDS, burn, trauma and cancer. Indeed, cachexia itself and not other effects of the tumor is thought to be the cause of up to 1/3 of all cancer deaths. Relatively little is understood regarding the molecular and cellular pathways leading to weight loss and dysmetabolism in cachexia and currently there are no approved, effective therapies. My group, working with a large and diverse group of collaborators, seeks to fill that knowledge gap by using novel animal models and correlative phenotypic and molecular data from patients to identify molecular, cellular and organ system mechanisms leading to cachexia. In this fashion we have:. 1. Identified a key role for IL-6/GP80/GP130/STAT3 in muscle and fat wasting in cancer and burns.. 2. Identified a causal role for Activins in burn-induced muscle wasting and shown efficacy in targeting ...

Follistatin is a single-chain gonadal protein that specifically inhibits follicle-stimulating hormone release. The single FST gene encodes two isoforms, FST317 and FST344 containing 317 and 344 amino acids respectively, resulting from alternative splicing of the precursor mRNA. In a study in which 37 candidate genes were tested for linkage and association with polycystic ovary syndrome (PCOS) or hyperandrogenemia in 150 families, evidence was found for linkage between PCOS and follistatin. [provided by RefSeq, Jul 2008]

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