Forskolin for increased height (1 Viewer)

[fent]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.

idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

 

[coloringhalo]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
View attachment 38192
View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

nice

 

[Hyporoxin]

will read later. nice though

 

[guilty]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
View attachment 38192
View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

mirin the effort

 

[Biomaxx]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
View attachment 38192
View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

Bm, will read when home

 

[fent]

bump

 

[Biomaxx]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
View attachment 38192
View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

Great read, would synergies well with a lower dose of abalo

 

[Perfectionist]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
View attachment 38192
View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

DNR but mirin the efforts bhai

 

[fent]

Great read, would synergies well with a lower dose of abalo

also check pms

 

[Synapse]

ill read later

 

[fent]

ill read later

forgot to @ you

 

[fent]

one more bump

 

[Mikey]

cool thread

 

[Veridic]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
View attachment 38192
View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

Cool thread but every day I see another post about a minimally studied "growth" compound with nobody ever actually having tried it out themselves

 

[tmpll]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
View attachment 38192
View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

nice thread

 

[fent]

Cool thread but every day I see another post about a minimally studied "growth" compound with nobody ever actually having tried it out themselves

ill probally run it with my stack if i can and when i do so give doccumentation.

 

[XvideosDemon]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
View attachment 38192
View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

nice thread bhai

love the name and avi ❤

 

[Dexter]

It also increases energy demand for the growth plates

vague extrapolation. increased cAMP signaling can stimulate cellular metabolism n activity like protein synthesis, i doubt you can simply frame it as "oh it increases energy demands of growth plate"

Stimulates IGF1 synthesis

this is dependant on context. cAMP/PKA signaling can influence transcription of many genes but forskolin's effects would prolly be systemic and unregulated unlike how controlled the pulsatile release of GH is that actually bumps IGF1 prod.. Theoretically this makes sense but practically its a maybe

Increases sox9 and cGMP

SOX9 sure, but im pretty sure the cGMP part is just wrong
the entire pathway described is the camp/pka pathway. cGMP is a different cyclic nucleotide and its part of the nitric oxide signaling pathway and acts thru protein kinase G, i doubt forskolin increase cGMP

 

[Hexum]

one more bump

2 more bumps

 

[fent]

vague extrapolation. increased cAMP signaling can stimulate cellular metabolism n activity like protein synthesis, i doubt you can simply frame it as "oh it increases energy demands of growth plate"

this is dependant on context. cAMP/PKA signaling can influence transcription of many genes but forskolin's effects would prolly be systemic and unregulated unlike how controlled the pulsatile release of GH is that actually bumps IGF1 prod.. Theoretically this makes sense but practically its a maybe

SOX9 sure, but im pretty sure the cGMP part is just wrong
the entire pathway described is the camp/pka pathway. cGMP is a different cyclic nucleotide and its part of the nitric oxide signaling pathway and acts thru protein kinase G, i doubt forskolin increase cGMP

Im going to bed so ill try reply to the rest tmr, correct this if im wrong.

 

[fent]

vague extrapolation. increased cAMP signaling can stimulate cellular metabolism n activity like protein synthesis, i doubt you can simply frame it as "oh it increases energy demands of growth plate"

this is dependant on context. cAMP/PKA signaling can influence transcription of many genes but forskolin's effects would prolly be systemic and unregulated unlike how controlled the pulsatile release of GH is that actually bumps IGF1 prod.. Theoretically this makes sense but practically its a maybe

SOX9 sure, but im pretty sure the cGMP part is just wrong
the entire pathway described is the camp/pka pathway. cGMP is a different cyclic nucleotide and its part of the nitric oxide signaling pathway and acts thru protein kinase G, i doubt forskolin increase cGMP

forskolin doesn’t directly use energy, but it stimulates growth processes that make growth plate cells need more energy.

 

[fent]

vague extrapolation. increased cAMP signaling can stimulate cellular metabolism n activity like protein synthesis, i doubt you can simply frame it as "oh it increases energy demands of growth plate"

this is dependant on context. cAMP/PKA signaling can influence transcription of many genes but forskolin's effects would prolly be systemic and unregulated unlike how controlled the pulsatile release of GH is that actually bumps IGF1 prod.. Theoretically this makes sense but practically its a maybe

SOX9 sure, but im pretty sure the cGMP part is just wrong
the entire pathway described is the camp/pka pathway. cGMP is a different cyclic nucleotide and its part of the nitric oxide signaling pathway and acts thru protein kinase G, i doubt forskolin increase cGMP

my bad the last part was wrong, you're right forskolin doesnt increase cGMP meaningfully

 

[jamc]

What is forskolin?

---

Forskolin is a natural compound extracted from the roots of the plant Coleus forskohlii, which belongs to the mint family. It has been used for centuries in traditional herbal medicine

---

How does it work?

---

Forskolin is known for its effect on a cellular process involving a molecule called cAMP (cyclic adenosine monophosphate). By increasing cAMP levels, it can influence several functions in the body.
Forskolin directly activates adenylyl cyclase wherever the enzyme is expressed in the cell, rather than relying on receptor-mediated pathways.
It also increases energy demand for the growth plates
Stimulates IGF1 synthesis
Increases membrane water permeability in cells.
Inhibits degradation of the growth plate extracellular matrix.
Increases sox9 and cGMP
Shown to increase testostrone as cAMP uses LH and FSH


Why does this matter?

---

First you need to understand PTHrP

What is PTHrp and how does it affect bone maturation?

---

PTHrP binds to the PTH1R receptor, causing a conformational change that activates heterotrimeric Gs proteins. These Gs proteins then stimulate adenylyl cyclase (AC), leading to the production of cAMP.
PTH1R. This phosphorylation recruits β-arrestin, which facilitates internalization of the receptor via clathrin-coated pits. Once internalized, PTH1R remains associated with PTHrP and Gs proteins, allowing continued activation of endosomal AC6 and sustained cAMP generation. AKAPs then position PKA near the nucleus. cAMP binds to the cyclic nucleotide–binding domains on the regulatory (R) subunits of PKA, causing release of the catalytic (C) subunits. These catalytic subunits phosphorylate SIK1/2/3, enabling HDAC4 to access its binding sites.


PKA-mediated phosphorylation inhibits SIKs, creating docking sites for 14-3-3 proteins. This interaction relocates SIKs to the cytoplasm, preventing them from inhibiting HDAC4/5. PP2A removes phosphate groups from HDAC4, allowing it to bind DNA and suppress the MEF2 gene (where MEF2 promotes maturation).


After this stage, CREB (cAMP response element-binding protein) is phosphorylated by PKA and binds directly to the SOX9 promoter. It also recruits p300, promoting chromatin accessibility for SOX9 and collagen type II (Col2) aggregation. Additionally, CREB recruits p300 to the Zfp521 gene promoter, increasing its mRNA expression. Elevated Zfp521 further inhibits maturation by binding to and inactivating Runx2, a key gene involved in maturation.
Overall, PTHrP signaling delays hypertrophic differentiation and plays a key role in regulating the timing of bone maturation.

Forskolins overall effect

---

Overall, it dramatically lowers the amount of PTH needed to trigger a cAMP response by up to 30–100×, indicating an increase in cellular sensitivity.
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View attachment 38193



idea by guilty
honourable mentions, Biomaxx tmpll Mikey 6ft1Cheat FoidSlayer

i saw that tik tok too

 

[paracelsus]

dnr

just do mossad jumps for height

 

[oyopth31]

Mirin I also did a thread on forskolin, but i dident know this aspect of it.