EvoMuse presents...HUNG

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  1. I see the Js above, I think it's a hint.
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  2. Quote Originally Posted by dsade View Post
    I prescribe Priapismyl-L-Carnitine.
    He appreciates the effort
    It's Bea, fcker. Bea Mother****ing Arthur. Dammit........lol

    Serious Nutrition Solutions Rep
    •   
       


  3. Quote Originally Posted by dsade View Post
    The function of this is so incredibily complicated that a simple DHT topical won't do anything at all. It were that easy, anyone taking steroids would have a huge dong.

    You have connective tissue, smooth muscle, vascular tissue, myofascia (sort of), and so many other factors that have to be manipulated. I'm Just happy because I found what I believe to be the one maJor limiting factor, and how to manipulate it to get the desired results.
    That's funny. I don't seem to have any problem manipulating the tissues you speak of. I do it a couple times a day actually.

    Quote Originally Posted by ryane87 View Post
    You're waiting for anything to pop up
    I wait and wait. Sometimes I think I am about to get a stroke of luck and something good is about to go down, but it turns out to just be a c0ck tease. This project is inching toward the finish line I hope. It just seems to keep going back and forth, up and down, but nothing ever comes of it.

  4. Quote Originally Posted by dsade View Post
    I think it's been more than 5 hours...call a doctor.
    Ya to brag about your 5hr erection

  5. Quote Originally Posted by rtmilburn View Post
    Ya to brag about your 5hr erection
    Yeah really? Who would do this? People complain about everything. Oh, I can't get it up! Oh, I can't get it down! Geez.
    •   
       


  6. Quote Originally Posted by rtmilburn View Post
    Ya to brag about your 5hr erection
    I put a red shrink wrapper around it and ask her if she wants to drink a 5 hour penergy.
    Evolutionary Muse - Inspire to Evolve
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  7. Quote Originally Posted by dsade View Post
    I put a red shrink wrapper around it and ask her if she wants to drink a 5 hour penergy.
    Haha that made me piss myself a little

  8. What in the WORLD can this be?"

    Pathway Description:

    Transforming growth factor-β (TGF-β) superfamily signaling plays a critical role in the regulation of cell growth, differentiation, and development in a wide range of biological systems. In general, signaling is initiated with ligand-induced oligomerization of serine/threonine receptor kinases and phosphorylation of the cytoplasmic signaling molecules Smad2 and Smad3 for the TGF-β/activin pathway, or Smad1/5/9 for the bone morphogenetic protein (BMP) pathway. Carboxy-terminal phosphorylation of Smads by activated receptors results in their partnering with the common signaling transducer Smad4, and translocation to the nucleus. Activated Smads regulate diverse biological effects by partnering with transcription factors resulting in cell-state specific modulation of transcription. Inhibitory Smads, i.e. Smad6 and Smad7 antagonize activation of R-Smads. The expression of inhibitory Smads (I-Smads) 6 and 7 is induced by both activin/TGF-β and BMP signaling as part of a negative feedback loop. The stability of TGF-β family receptors and/or Smads are regulated by Smurf E3 ubiquitin ligases and USP4/11/15 deubiquitinases. TGF-β/activin and BMP pathways are modulated by MAPK signaling at a number of levels. Moreover, in certain contexts, TGF-β signaling can also affect Smad-independent pathways, including Erk, SAPK/JNK, and p38 MAPK pathways. Rho GTPase (RhoA) activates downstream target proteins, such as mDia and ROCK, to prompt rearrangement of the cytoskeletal elements associated with cell spreading, cell growth regulation, and cytokinesis. Cdc42/Rac regulates cell adhesion through downstream effector kinases PAK, PKC, and c-Abl following TGF-β activation.
    - See more at: https://www.cellsignal.com/contents/....u0PxWAbF.dpuf

    What do we see again that EvoMuse is pioneering?

    Oh yeah...how are we going to trigger cellular proliferation?

    Planta Med. 2013 May;79(8):616-21. doi: 10.1055/s-0032-1328364. Epub 2013 Apr 8.
    Effect of topical application of chlorogenic acid on excision wound healing in rats.
    Chen WC1, Liou SS, Tzeng TF, Lee SL, Liu IM.
    Author information
    Abstract

    This study was undertaken to evaluate the therapeutic effects of topical chlorogenic acid on excision wounds in Wistar rats. A 1 % (w/w) chlorogenic acid or silver sulfadiazine ointment was applied topically once a day for 15 days on full-thickness excision wounds created on rats. The 1 % (w/w) chlorogenic acid ointment had potent wound healing capacity as evident from the wound contraction on the 15th post-surgery day, which was similar to that produced by 1 % (w/w) silver sulfadiazine ointment. Increased rates of epithelialization were observed in the treated rats. It also improved cellular proliferation, increased tumor necrosis factor-α levels during the inflammatory phase (12 h, 24 h, 48 h, and 72 h post-wounding) of wound healing, upregulated transforming growth factor-β1 and elevated collagen IV synthesis in the chlorogenic acid-treated group. The results also indicated that chlorogenic acid possesses potent antioxidant activity by increasing superoxide dismutase, catalase, and glutathione, and decreasing lipid peroxidation. In conclusion, these results demonstrate that topical application of chlorogenic acid can accelerate the process of excision wound healing by its ability to increase collagen synthesis through upregulation of key players such as tumor necrosis factor-α and transforming growth factor-β1 in different phases of wound healing as well as by its antioxidant potential.

    Georg Thieme Verlag KG Stuttgart ∑ New York.

    PMID:
    23568627
    Evolutionary Muse - Inspire to Evolve
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  9. Now what happens when we mechanically "inJure" critical ligaments, as well as size limiting fascia?
    Evolutionary Muse - Inspire to Evolve
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  10. Quote Originally Posted by dsade View Post
    What in the WORLD can this be?"

    Pathway Description:

    Transforming growth factor-β (TGF-β) superfamily signaling plays a critical role in the regulation of cell growth, differentiation, and development in a wide range of biological systems. In general, signaling is initiated with ligand-induced oligomerization of serine/threonine receptor kinases and phosphorylation of the cytoplasmic signaling molecules Smad2 and Smad3 for the TGF-β/activin pathway, or Smad1/5/9 for the bone morphogenetic protein (BMP) pathway. Carboxy-terminal phosphorylation of Smads by activated receptors results in their partnering with the common signaling transducer Smad4, and translocation to the nucleus. Activated Smads regulate diverse biological effects by partnering with transcription factors resulting in cell-state specific modulation of transcription. Inhibitory Smads, i.e. Smad6 and Smad7 antagonize activation of R-Smads. The expression of inhibitory Smads (I-Smads) 6 and 7 is induced by both activin/TGF-β and BMP signaling as part of a negative feedback loop. The stability of TGF-β family receptors and/or Smads are regulated by Smurf E3 ubiquitin ligases and USP4/11/15 deubiquitinases. TGF-β/activin and BMP pathways are modulated by MAPK signaling at a number of levels. Moreover, in certain contexts, TGF-β signaling can also affect Smad-independent pathways, including Erk, SAPK/JNK, and p38 MAPK pathways. Rho GTPase (RhoA) activates downstream target proteins, such as mDia and ROCK, to prompt rearrangement of the cytoskeletal elements associated with cell spreading, cell growth regulation, and cytokinesis. Cdc42/Rac regulates cell adhesion through downstream effector kinases PAK, PKC, and c-Abl following TGF-β activation.
    - See more at: https://www.cellsignal.com/contents/....u0PxWAbF.dpuf

    What do we see again that EvoMuse is pioneering?

    Oh yeah...how are we going to trigger cellular proliferation?

    Planta Med. 2013 May;79(8):616-21. doi: 10.1055/s-0032-1328364. Epub 2013 Apr 8.
    Effect of topical application of chlorogenic acid on excision wound healing in rats.
    Chen WC1, Liou SS, Tzeng TF, Lee SL, Liu IM.
    Author information
    Abstract

    This study was undertaken to evaluate the therapeutic effects of topical chlorogenic acid on excision wounds in Wistar rats. A 1 % (w/w) chlorogenic acid or silver sulfadiazine ointment was applied topically once a day for 15 days on full-thickness excision wounds created on rats. The 1 % (w/w) chlorogenic acid ointment had potent wound healing capacity as evident from the wound contraction on the 15th post-surgery day, which was similar to that produced by 1 % (w/w) silver sulfadiazine ointment. Increased rates of epithelialization were observed in the treated rats. It also improved cellular proliferation, increased tumor necrosis factor-α levels during the inflammatory phase (12 h, 24 h, 48 h, and 72 h post-wounding) of wound healing, upregulated transforming growth factor-β1 and elevated collagen IV synthesis in the chlorogenic acid-treated group. The results also indicated that chlorogenic acid possesses potent antioxidant activity by increasing superoxide dismutase, catalase, and glutathione, and decreasing lipid peroxidation. In conclusion, these results demonstrate that topical application of chlorogenic acid can accelerate the process of excision wound healing by its ability to increase collagen synthesis through upregulation of key players such as tumor necrosis factor-α and transforming growth factor-β1 in different phases of wound healing as well as by its antioxidant potential.

    Georg Thieme Verlag KG Stuttgart ∑ New York.

    PMID:
    23568627
    Come on man! Science? More talk about "manipulation". I don't really understand a word you just said.

  11. Quote Originally Posted by dsade View Post
    What in the WORLD can this be?"

    Pathway Description:

    Transforming growth factor-β (TGF-β) superfamily signaling plays a critical role in the regulation of cell growth, differentiation, and development in a wide range of biological systems. In general, signaling is initiated with ligand-induced oligomerization of serine/threonine receptor kinases and phosphorylation of the cytoplasmic signaling molecules Smad2 and Smad3 for the TGF-β/activin pathway, or Smad1/5/9 for the bone morphogenetic protein (BMP) pathway. Carboxy-terminal phosphorylation of Smads by activated receptors results in their partnering with the common signaling transducer Smad4, and translocation to the nucleus. Activated Smads regulate diverse biological effects by partnering with transcription factors resulting in cell-state specific modulation of transcription. Inhibitory Smads, i.e. Smad6 and Smad7 antagonize activation of R-Smads. The expression of inhibitory Smads (I-Smads) 6 and 7 is induced by both activin/TGF-β and BMP signaling as part of a negative feedback loop. The stability of TGF-β family receptors and/or Smads are regulated by Smurf E3 ubiquitin ligases and USP4/11/15 deubiquitinases. TGF-β/activin and BMP pathways are modulated by MAPK signaling at a number of levels. Moreover, in certain contexts, TGF-β signaling can also affect Smad-independent pathways, including Erk, SAPK/JNK, and p38 MAPK pathways. Rho GTPase (RhoA) activates downstream target proteins, such as mDia and ROCK, to prompt rearrangement of the cytoskeletal elements associated with cell spreading, cell growth regulation, and cytokinesis. Cdc42/Rac regulates cell adhesion through downstream effector kinases PAK, PKC, and c-Abl following TGF-β activation.
    - See more at: https://www.cellsignal.com/contents/....u0PxWAbF.dpuf

    What do we see again that EvoMuse is pioneering?

    Oh yeah...how are we going to trigger cellular proliferation?

    Planta Med. 2013 May;79(8):616-21. doi: 10.1055/s-0032-1328364. Epub 2013 Apr 8.
    Effect of topical application of chlorogenic acid on excision wound healing in rats.
    Chen WC1, Liou SS, Tzeng TF, Lee SL, Liu IM.
    Author information
    Abstract

    This study was undertaken to evaluate the therapeutic effects of topical chlorogenic acid on excision wounds in Wistar rats. A 1 % (w/w) chlorogenic acid or silver sulfadiazine ointment was applied topically once a day for 15 days on full-thickness excision wounds created on rats. The 1 % (w/w) chlorogenic acid ointment had potent wound healing capacity as evident from the wound contraction on the 15th post-surgery day, which was similar to that produced by 1 % (w/w) silver sulfadiazine ointment. Increased rates of epithelialization were observed in the treated rats. It also improved cellular proliferation, increased tumor necrosis factor-α levels during the inflammatory phase (12 h, 24 h, 48 h, and 72 h post-wounding) of wound healing, upregulated transforming growth factor-β1 and elevated collagen IV synthesis in the chlorogenic acid-treated group. The results also indicated that chlorogenic acid possesses potent antioxidant activity by increasing superoxide dismutase, catalase, and glutathione, and decreasing lipid peroxidation. In conclusion, these results demonstrate that topical application of chlorogenic acid can accelerate the process of excision wound healing by its ability to increase collagen synthesis through upregulation of key players such as tumor necrosis factor-α and transforming growth factor-β1 in different phases of wound healing as well as by its antioxidant potential.

    Georg Thieme Verlag KG Stuttgart ∑ New York.

    PMID:
    23568627
    Haha nice literally read this an hour ago

  12. Damn..perhaps a smidge too big, perhaps not. I got beta-escin to penetrate in the 800s, but then again escin has it's own penetration enhancement weaponds that might lead the way for the collagen hydroiysates.

    Pathway Description:

    Transforming growth factor-β (TGF-β) superfamily signaling plays a critical role in the regulation of cell growth, differentiation, and development in a wide range of biological systems. In general, signaling is initiated with ligand-induced oligomerization of serine/threonine receptor kinases and phosphorylation of the cytoplasmic signaling molecules Smad2 and Smad3 for the TGF-β/activin pathway, or Smad1/5/9 for the bone morphogenetic protein (BMP) pathway. Carboxy-terminal phosphorylation of Smads by activated receptors results in their partnering with the common signaling transducer Smad4, and translocation to the nucleus. Activated Smads regulate diverse biological effects by partnering with transcription factors resulting in cell-state specific modulation of transcription. Inhibitory Smads, i.e. Smad6 and Smad7 antagonize activation of R-Smads. The expression of inhibitory Smads (I-Smads) 6 and 7 is induced by both activin/TGF-β and BMP signaling as part of a negative feedback loop. The stability of TGF-β family receptors and/or Smads are regulated by Smurf E3 ubiquitin ligases and USP4/11/15 deubiquitinases. TGF-β/activin and BMP pathways are modulated by MAPK signaling at a number of levels. Moreover, in certain contexts, TGF-β signaling can also affect Smad-independent pathways, including Erk, SAPK/JNK, and p38 MAPK pathways. Rho GTPase (RhoA) activates downstream target proteins, such as mDia and ROCK, to prompt rearrangement of the cytoskeletal elements associated with cell spreading, cell growth regulation, and cytokinesis. Cdc42/Rac regulates cell adhesion through downstream effector kinases PAK, PKC, and c-Abl following TGF-β activation.
    Evolutionary Muse - Inspire to Evolve
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  13. Quote Originally Posted by dsade View Post
    This space intentionally left blank.

    Let's see who remembers...Where are my old M&M peeps?
    Present. lol.

  14. Quote Originally Posted by Cordeen View Post
    Present. lol.
    I remember M&M 👋✋

  15. Ok a little more teasing and updates for those following along scientifically.

    https://www.ncbi.nlm.nih.gov/pubmed/28085667


    Significance

    Birth defects of external genitalia occur at a striking frequency, affecting ∼1:250 live births. Congenital penile anomalies (CPAs) encompass a range of malformations, including failure of urethral tube closure (hypospadias), penile curvature (chordee), micropenis, and feminization of male genitalia. Both genetic anomalies and exposures to endocrine disrupting chemicals (EDCs) are suspected to be involved; however, little is known about the underlying causes or the developmental window(s) of sensitivity to antiandrogenic or estrogenic signals. This study shows that disruption of androgen signaling at different stages of genital development can induce different types of CPA. We identify a cell type in which the androgen receptor (AR) is essential for genital masculinization and uncover previously unknown mechanisms through which antiandrogenic and estrogenic signals induce penile malformations.


    Estrogenic signalling:
    https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Citation
    Sci Rep, 2016 vol. 6

    Effect of the Interaction of Veratrum Nigrum with Panax Ginseng on Estrogenic Activity In Vivo and In Vitro.

    Xu, Y; Ding, J; An, Jn; Qu, Yk; Li, X; Ma, Xp; Zhang, Ym; Dai, Gj; Lin, N

    Panax ginseng (GS) and Veratrum nigrum (VN) are representative of incompatible pairs in “eighteen antagonistic medicaments” that have been recorded in the Chinese medicinal literature for over 2,000 years. However, evidence linking interference effects with combination use is scare. Based on the estrogen-like effect of GS described in our previous studies, we undertake a characterization of the interaction on estrogenic activity of GS and VN using in vivo models of immature and ovariectomized (OVX) mice and in vitro studies with MCF-7 cells for further mechanism. VN decreased the estrogenic efficacy of GS on promoting the development of the uterus and vagina in immature mice, and reversing the atrophy of reproductive tissues in OVX mice. VN interfered with the estrogenic efficacy of GS by decreasing the increase of the serum estradiol and the up-regulation of ERα and ERβ expressions by treatment with GS. And VN antagonized the estrogenic efficacy of GS on promoting the viability of MCF-7 cells and up-regulation of protein and gene expressions of ERs. In conclusion, this study provided evidence that GS and VN decreased effects on estrogenic activity, which might be related to regulation of estrogen secretion and ERs.

    PMID: 27229740

    PMCID: PMC4882595

    ANDROGENIC SIGNALING:

    From the testruction writeup, we know that E Ulmoides amplifies hormone signaling at the receptor. So we have Veratrum nigrum to interfere with the estrogenic signaling (hmm, seems like this would be a good addition to Elimistane) leaving E. Ulmoides to amplify androgenic signaling. One piece of the puzzle hopefully solved...the androgenic receptor. We still have a TON of work to do until this beast of a formula is done.
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  16. To reinforce the above:

    http://www.pnas.org/content/112/52/E7194.full

    Significance

    Birth defects of external genitalia occur at a striking frequency, affecting ∼1:250 live births. Congenital penile anomalies (CPAs) encompass a range of malformations, including failure of urethral tube closure (hypospadias), penile curvature (chordee), micropenis, and feminization of male genitalia. Both genetic anomalies and exposures to endocrine disrupting chemicals (EDCs) are suspected to be involved; however, little is known about the underlying causes or the developmental window(s) of sensitivity to antiandrogenic or estrogenic signals. This study shows that disruption of androgen signaling at different stages of genital development can induce different types of CPA. We identify a cell type in which the androgen receptor (AR) is essential for genital masculinization and uncover previously unknown mechanisms through which antiandrogenic and estrogenic signals induce penile malformations.


    Now, to simulate the state of being in development we're hoping that recruiting of stem cells can be maniulated like the cells of growing fetuses.

    {saved for the study I can't find}


    As well, this pathway as well as the WNT/c-Catenin pathway are important growth signaling pathways.

    https://www.ncbi.nlm.nih.gov/pubmed/28085667

    Significance

    Elife. 2017 Jan 13;6. pii: e21049. doi: 10.7554/eLife.21049.
    Proliferation-independent regulation of organ size by Fgf/Notch signaling.
    Kozlovskaja-Gumbrienė A1, Yi R1, Alexander R1, Aman A1, Jiskra R1, Nagelberg D2, Knaut H2, McClain M1, Piotrowski T1.
    Author information
    Abstract

    Organ morphogenesis depends on the precise orchestration of cell migration, cell shape changes and cell adhesion. We demonstrate that Notch signaling is an integral part of the Wnt and Fgf signaling feedback loop coordinating cell migration and the self-organization of rosette-shaped sensory organs in the zebrafish lateral line system. We show that Notch signaling acts downstream of Fgf signaling to not only inhibit hair cell differentiation but also to induce and maintain stable epithelial rosettes. Ectopic Notch expression causes a significant increase in organ size independently of proliferation and the Hippo pathway. Transplantation and RNASeq analyses revealed that Notch signaling induces apical junctional complex genes that regulate cell adhesion and apical constriction. Our analysis also demonstrates that in the absence of patterning cues normally provided by a Wnt/Fgf signaling system, rosettes still self-organize in the presence of Notch signaling.
    KEYWORDS:

    Hippo pathway; apical constriction; cell adhesion; cell biology; collective cell migration; developmental biology; lateral line system; rosettes; stem cells; zebrafish

    PMID:
    28085667

    TGF-B

    Tranforming Growth Factor beta increases in adulthood while adrogen receptors down-regulate. We don't want that, we want that tissue nice and rich in hungry androgen receptors. Inhibition of TGF-b allows for growth to happen with the right stiimulus.

    https://www.ncbi.nlm.nih.gov/pubmed/9537291

    J Androl. 1998 Jan-Feb;19(1):50-7.
    Transforming growth factor-beta1 (TGF-beta1) in penile and prostate growth in the rat during sexual maturation.
    Gelman J1, GarbŠn H, Shen R, Ng C, Cai L, Rajfer J, Gonzalez-Cadavid NF.
    Author information
    Abstract

    The goal of this study was to determine whether transforming growth factor-beta1 (TGF-beta1) may contribute to the arrest of penile growth and the down-regulation of androgen receptors (AR) that occur during sexual maturation in the rat penis. For this purpose, body, penis, and prostate weights were obtained from male rats of increasing ages, and penis and prostate TGF-beta1 concentrations were determined by a sandwich enzyme-linked immunosorbent assay. The cytosol fraction was obtained from the shafts and glandes of immature (19-day-old) and adult (90-day-old) rat penises, and ARs were measured by a western blot assay. The effect of exogenous TGF-beta1 on penile growth was examined in vivo in two groups of immature rats (21 and 27 days old) implanted with miniosmotic pumps delivering either human TGF-beta1 or vehicle only directly into the corpora cavernosa for 6 days. The penises, prostates, and testes were weighed, and the AR content was estimated by western blot. The growth rate of the penis declined after 8 weeks of age, whereas the ventral prostate growth rate increased until 14 weeks of age and then slowed down. The content of penile AR protein decreased seven-fold in the adult rats compared to the immature animals. Penile TGF-beta1 concentration increased nearly three-fold from the 19-day-old rats to a peak at 60 days of age and then decreased over the next 4 months to the initial levels. In contrast, TGF-beta1 concentration in the prostate was not significantly affected by age and remained below the lowest penile values in all age groups. Transforming growth factor-beta1 given locally to the penis reduced penile shaft weight by 38 and 22% in two groups of immature rats, while the weights of the penile glans, testis, and ventral prostate remained unaffected. Androgen receptor content was higher in the glans than in the shaft and was not changed by TGF-beta1 treatment. These results suggest that the increase of TGF-beta1 levels in the penis may reinforce growth arrest caused by the down-regulation of penile ARs, whereas the maintenance of a high content of ARs and a low TGF-beta1 concentration may allow prostate growth to continue.

    PMID:
    9537291
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  17. But it's not that simple....

    Journal of Cell Science 2004 117: 4377-4388; doi: 10.1242/jcs.01291

    ArticleFigures & tablesSupp infoInfo & metrics
    PDF + SI
    PDF

    Summary

    Mesoangioblasts are vessel-derived stem cells that can be induced to differentiate into different cell types of the mesoderm such as muscle and bone. The gene expression profile of four clonal derived lines of mesoangioblasts was determined by DNA micro-array analysis: it was similar in the four lines but different from 10T1/2 embryonic fibroblasts, used as comparison. Many known genes expressed by mesoangioblasts belong to response pathways to developmental signalling molecules, such as Wnt or TGFβ/BMP. Interestingly, mesoangioblasts express receptors of the TGFβ/BMP family and several Smads and, accordingly, differentiate very efficiently into smooth muscle cells in response to TGFβ and into osteoblasts in response to BMP. In addition, insulin signalling promotes adipogenic differentiation, possibly through the activation of IGF-R. Several Wnts and Frizzled, Dishevelled and Tcfs are expressed, suggesting the existence of an autocrine loop for proliferation and indeed, forced expression of Frzb-1 inhibits cell division. Mesoangioblasts also express many neuro-ectodermal genes and yet undergo only abortive neurogenesis, even after forced expression of neurogenin 1 or 2, MASH or NeuroD. Finally, mesoangioblasts express several pro-inflammatory genes, cytokines and cytokine receptors, which may explain their ability to be recruited by tissue inflammation. Our data define a unique phenotype for mesoangioblasts, explain several of their biological features and set the basis for future functional studies on the role of these cells in tissue histogenesis and repair.

    http://jcs.biologists.org/content/117/19/4377


    Notch:



    Segregation of striated and smooth muscle lineages by a Notch-dependent regulatory network

    PubMed Central

    2014-01-01

    Background Lineage segregation from multipotent epithelia is a central theme in development and in adult stem cell plasticity. Previously, we demonstrated that striated and smooth muscle cells share a common progenitor within their epithelium of origin, the lateral domain of the somite-derived dermomyotome. However, what controls the segregation of these muscle subtypes remains unknown. We use this in vivo bifurcation of fates as an experimental model to uncover the underlying mechanisms of lineage diversification from bipotent progenitors. Results Using the strength of spatio-temporally controlled gene missexpression in avian embryos, we report that Notch harbors distinct pro-smooth muscle activities depending on the duration of the signal; short periods prevent striated muscle development and extended periods, through Snail1, promote cell emigration from the dermomyotome towards a smooth muscle fate. Furthermore, we define a Muscle Regulatory Network, consisting of Id2, Id3, FoxC2 and Snail1, which acts in concert to promote smooth muscle by antagonizing the pro-myogenic activities of Myf5 and Pax7, which induce striated muscle fate. Notch and BMP closely regulate the network and reciprocally reinforce each other‚€™s signal. In turn, components of the network strengthen Notch signaling, while Pax7 silences this signaling. These feedbacks augment the robustness and flexibility of the network regulating muscle subtype segregation. Conclusions Our results demarcate the details of the Muscle Regulatory Network, underlying the segregation of muscle sublineages from the lateral dermomyotome, and exhibit how factors within the network promote the smooth muscle at the expense of the striated muscle fate. This network acts as an exemplar demonstrating how lineage segregation occurs within epithelial primordia by integrating inputs from competing factors. PMID:25015411


    {SAVED FOR BMP}
    {SAVED FOR VEGF}
    {SAVED FOR NGF}
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  18. Can you be more specific?

  19. Quote Originally Posted by Ricky10 View Post
    Can you be more specific?
    Not yet, and not publicly. I'm going to post enough to keep you guys sort of in the loop, and not enough to be ripped off.
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  20. Quote Originally Posted by dsade View Post
    Not yet, and not publicly. I'm going to post enough to keep you guys sort of in the loop, and not enough to be ripped off.
    I was kidding...haha!

    Lots of info!

  21. So are you giving me a bigger penis in 2017?

  22. Quote Originally Posted by Ape McGrapes View Post
    So are you giving me a bigger penis in 2017?
    Buy one get one free
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  23. Quote Originally Posted by dsade View Post
    Buy one get one free
    I do like a free dick

  24. Quote Originally Posted by dsade View Post
    Buy one get one free
    I trust this offer only applies to white dudes
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  25. Quote Originally Posted by GNO View Post
    I trust this offer only applies to white dudes
    Shipping would cost too much for BBC
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