Our latest work has been published in the Journal of Fluorine Chemistry! Many thanks to Dr. Morisako (@SMorisako) and to all co-authors/collaborators. "One-step formal dimerization of hexafluoropropylene oxide using K2CO3 and H2O as oxygen sources" sciencedirect.com/science/ar…

Lactobacillus Reuteri, the probiotic ppl gobble up for health benifits, has a "D-lactate induced site-specific STAT3 lactylation at lysine 631, thereby promoting STAT3 dimerization and nuclear translocation". This GMO version dosn't! pubmed.ncbi.nlm.nih.gov/4228… #digitalmicrobiome

Non-Hermitian scattering in SSH superconducting waveguides: exact Green-function reduction and dimerization-sensitive microwave functionalities Jie Zhou, Xiao-Xue Zhang, Xi-Zheng Zhang arxiv.org/abs/2606.10555 [𝚚𝚞𝚊𝚗𝚝-𝚙𝚑]

Nice work😆still wonder how cytoskeletal contractility reduction (ROCK inhibition) leads to phosphorylation of junctional EGFR? Reduced EGFR internalization? Reduced cortical actin thus less steric hindrance for EGFR dimerization?😆

Excited to share an updated preprint from our OC25 release last summer! We demonstrate how OC25-trained models enable large-scale, explicit-solvent simulations of electrocatalytic interfaces! Lots of exciting insights on CO dimerization on Cu! Preprint: arxiv.org/abs/2509.17862

On RXR: the paper focuses on FokI ff reducing VDR transcriptional efficiency, not RXR mutation or impaired dimerization. Less efficient VDR, same architecture. Your women’s model fits: estrogen as osteogenic driver until menopause, then the rescue fails. Men trade hair. Women trade bone.

Non-Hermitian scattering in SSH superconducting waveguides: exact Green-function reduction and dimerization-sensitive microwave functionalities arxiv.org/pdf/2606.10555 Jie Zhou, Xiao-Xue Zhang, Xi-Zheng Zhang. arxiv.org/abs/2606.10555

Diversity-driven biochemical survey reveals widespread dimerization throughout the rubisco superfamily | Nature Communications nature.com/articles/s41467-0…

Structural Evolution of LEAFY Reveals DNA-Mediated Cooperativity and Dimerization Shifts at the Water-to-Land Transition biorxiv.org/content/10.64898… ♻️

If you have healthy testosterone levels but you are still suffering from symptoms of hypogonadism, then your next step should be working on your androgen receptors. First and foremost, why does our body even need androgen receptors? Because the places where hormones are produced and the places that are utilized are not the same. So these receptors bridge the gap between hormone production (in the testes for example) and their action in distant tissues (the muscles for example). I hope that this was pretty simple. Now these intracellular proteins function as ligand-activated transcription factors and mediate the effects of androgens as you might be able to tell. They are expressed in a wide range of tissues such as the prostate, testes, seminal vesicles, epididymis, skeletal muscle, bones, hair follicles, sebaceous glands, hypothalamus, pituitary, liver, adipose tissue and cardiovascular system. So when we pair the effects of androgens with the tissues which ARs are expressed, we can better understand why their activation leads to sexual development, enhanced protein synthesis in muscles and osteoblast activity in bones, the regulation of lipid metabolism, insulin sensitivity, energy homeostasis but also how they modulate mood, cognition and sexual behavior (and plenty of other neurological effects (ARs in the hippocampus and amygdala for example greatly modulate stress-related behaviors)). ARs exist in an inactive state in the cytoplasm, bound to heat shock proteins (HSPs) and other chaperones, which stabilize it until ligand binding occurs. When it comes to the domains of ARs: -The N-terminal domain (NTD) contains activation function 1 (AF1), which is involved in transcriptional activation. It interacts with co-regulatory proteins to modulate gene expression. -The DNA-binding domain (DBD) contains zinc finger motifs that allow the receptor to bind to specific DNA sequences called androgen response elements (AREs) in the promoter regions of target genes. -The hinge region connects the DBD to the ligand-binding domain and contains a nuclear localization signal (NLS) to direct the receptor to the cell nucleus upon activation. -The ligand-binding domain (LBD) is located at the C-terminus, this domain forms a pocket that binds androgens with high specificity and affinity. It also contains activation function 2 (AF2), which is critical for recruiting co-activator proteins after ligand binding. Now chromosomes are structures in the nucleus of cells that carry genetic information in the form of DNA. Each chromosome contains many genes, and we typically have 46 chromosomes (23 pairs), including 22 pairs of autosomes (non-sex chromosomes) and one pair of sex chromosomes (XX for females and XY for males). Males (XY) inherit their single X chromosome (and X-linked genes) from their mother and the Y chromosome from their father. Females (XX): Inherit one X chromosome from each parent. Mitochondrial genes are also inherited solely from the mother, as mitochondria (and their DNA) come from the egg. Why do these matter? Because the AR gene, is located on the X chromosome (Xq11-12). Males, inherit their single AR gene from their mother’s X chromosome. The father contributes the Y chromosome, which lacks AR. Thus, for males, the androgen receptor is exclusively inherited from the mother’s side. Females, inherit one AR allele from the mother and one from the father (via his X chromosome). If these were too complicated here’s a brief summary of how androgen receptors work. A molecule of an androgen hormone slips through the cell’s outer membrane since it’s fat-soluble, it finds the androgen receptor and goes to the ligand-binding domain (LBD) in the cytoplasm. This causes the receptor to change shape and kick off the heat shock proteins (HSPs) in order to expose parts of the receptor that were hidden. Once activated, it travels to the cell’s nucleus with the help of nuclear localization signal (NLS) in order to influence the cell’s instructions (DNA is stored in the nucleus). Once in the nucleus, two activated receptors “team up” (just an analogy for dimerization) to form a “homodimer” which then binds to specific spots on the DNA called androgen response elements (AREs). In order to modulate gene expression, the receptor needs help from other proteins called co-activators or co-repressors that “open up” the DNA (by adding chemical tags to histones, which are like spools that DNA is wrapped around) or “close it off” to control whether genes are turned on or off. They also connect the receptor to the cell’s machinery that reads DNA. Then all these instruct the cell to make specific proteins by turning on or off certain genes, which then carry out the androgen’s effects. In order to understand how we can have healthy ARs and improve their function, we must remember that the activity of ARs is regulated by: -Ligand availability (controlled by enzymes like 5α-reductase and aromatase). -Co-activators such as SRC-1 and CBP/p300. -Co-repressors such as NCoR and SMRT. -Phosphorylation, acetylation and ubiquitination -Feedback mechanisms: Androgen signaling regulates the hypothalamic-pituitary-gonadal axis, controlling testosterone production. Now based on these, here's how you can support your androgen receptors. Ground zero: Wok on testosterone and overall androgen levels and manage estrogen. ncbi.nlm.nih.gov/pubmed/1455… Even DHEA for example can increase ARs. Number 1: Fix your sleep and circadian rhythm. Poor sleep impairs testosterone production and AR expression through multiple mechanisms. It reduces testosterone production in Leydig cells for example, downregulates AR expression and lowers luteinizing hormone (LH) pulses. Number 2: Relax/manage cortisol. Chronic stress elevates cortisol, which can suppress AR sensitivity by competing with androgen signaling pathways, as cortisol binds to glucocorticoid receptors (GR) that interact with ARs. Adaptogens such as rhodiola or holy basil might also help to reduce cortisol in some people. Number 3: Get sunlight and go measure your vitamin D levels. Vitamin D not only enhances testosterone production but also boosts AR function. Number 4: Avoid digital overstimulation. Chronic overstimulation which is very easily accomplished these days through digital means, may deplete dopamine levels and desensitize dopamine receptors (D1/D2) in reward-related brain regions like the nucleus accumbens. Basically, by causing these unnatural dopamine spikes frequently, we are downregulating dopamine receptors and the problem is that dopamine signaling is linked to AR function. Try a combat sport instead of scrolling.pmc.ncbi.nlm.nih.gov/article… Number 5: Avoid endocrine-disrupting chemicals Things such as bisphenol A (BPA), phthalates and pesticides not only bind to AR as antagonists, preventing androgen binding, disrupting testosterone synthesis by inhibiting steroidogenic enzymes in Leydig cells but they also alter AR expression. Number 6: Regulate proinflammatory cytokines. Pro-inflammatory cytokines such as TNF-α and IL-6, suppress AR function by downregulating AR expression, increasing cortisol production and disrupting testosterone synthesis. Number 7: Avoid heavy metal exposure. Heavy metals bind to ARs and act as antagonists and inhibit testosterone synthesis through toxicity to Leydig cells (cadmium for example mimics estrogen). Number 8: Get a wide range of micronutrients. Deficiencies in key nutrients like zinc, magnesium, B vitamins, selenium and potassium impair AR function. But just like everything, an excess has the exact opposite effect so prioritize whole food sources over supplements when it comes to covering your baseline needs. Number 9: Avoid excessive alcohol consumption. Chronic or excessive alcohol intake disrupts AR function by suppressing testosterone production through inhibition of LH and steroidogenic enzymes, increasing oxidative stress, which impairs AR signaling, and promoting aromatization of testosterone to estrogen, reducing androgen availability. Number 10: Heal your gut An imbalanced gut microbiome (dysbiosis) can impair AR function by increasing systemic inflammation via leaky gut, which elevates cytokines that suppress AR, reducing short-chain fatty acid (SCFA) production which supports testosterone synthesis, and altering bile acid metabolism, which influences steroid hormone regulation. Gut bacteria also modulate estrogen metabolism, and dysbiosis may increase estrogen levels, reducing androgen availability. Number 11: Support your thyroid. ncbi.nlm.nih.gov/pubmed/8568… Number 12: Fix your mitochondria. Mitochondria are critical for cellular energy production (ATP via oxidative phosphorylation, OXPHOS) and steroidogenesis (testosterone synthesis in Leydig cells). Number 13: Go train. Training is taken for granted a lot of the time, but it’s one of the fundamental aspects of hormonal health that should never be neglected. pubmed.ncbi.nlm.nih.gov/1942… ncbi.nlm.nih.gov/pubmed/1535… Number 15: Eat post workout and do not eat right before going to bed. ncbi.nlm.nih.gov/pubmed/1682… Number 16: Do not use NSAIDs (aspirin can be excluded from this) for no real reason. pubmed.ncbi.nlm.nih.gov/1291… Number 17: Consider ALCAR or niacinamide if your methylation status is fine. There are other supplements that can help such as forskolin, tribulus and maybe even lithium orotate for example. But if you are just starting out stick with ALCAR since it’s a better bang for your buck and forskolin needs regular blood work, tribulus will make more people hypomanic compared to ALCAR and lithium orotate interacts with a lot of medications and will blunt emotions for some people. I am not saying that these are useless, but i am saying that ALCAR is a better starting point. ncbi.nlm.nih.gov/pubmed/1999… That's it. For more on all of these, go here for a few more hours: fitandball.gumroad.com/l/geo… -George

Diversity-driven biochemical survey reveals widespread dimerization throughout the rubisco superfamily nature.com/articles/s41467-0… @NatureComms

Publication - by Dr. Peter Chi and Hsin-Yung Yen @ACSPublications #Helicase-like #transcription factor (HLTF) involves in #DNA replication fork reversal. This study reveals the ATP-induced dimerization of HLTF and its role in DNA unwinding activity. doi.org/10.1021/jacs.5c22675

Upon binding, the FGFRs undergo dimerization, bringing their intracellular tyrosine kinase domains into close proximity. Finally, these activated domains utilize ATP to phosphorylate the receptor dimer, triggering downstream cellular responses.

"Why shouldn't i just use finasteride?". I'm glad you asked. Post finasteride syndrome is more real than most men would want it to be. Here are some example when it comes to why it can ruin your life as a man: 1. Finasteride reduces the conversion of testosterone to dihydrotestosterone (DHT) and these effects on androgen signaling influence AR function and related pathways. In case it's unclear: DHT has a higher affinity for ARs than testosterone (2–10 times stronger binding) and thus by inhibiting 5α-reductase it reduces AR activation. 2. Since ARs regulate gene expression through binding to androgen response elements (AREs) finasteride result in decreased transcription of DHT-dependent genes. 3. Reduced DHT levels can disrupt the hypothalamic-pituitary-gonadal (HPG) axis. So it giga fries your androgen receptors. Why does our body even need androgen receptors? Because the places where hormones are produced and the places that are utilized are not the same. So these receptors bridge the gap between hormone production (in the testes for example) and their action in distant tissues (the muscles for example). I hope that this was pretty simple. Now these intracellular proteins function as ligand-activated transcription factors and mediate the effects of androgens as you might be able to tell. They are expressed in a wide range of tissues such as the prostate, testes, seminal vesicles, epididymis, skeletal muscle, bones, hair follicles, sebaceous glands, hypothalamus, pituitary, liver, adipose tissue and cardiovascular system. So when we pair the effects of androgens with the tissues which ARs are expressed, we can better understand why their activation leads to sexual development, enhanced protein synthesis in muscles and osteoblast activity in bones, the regulation of lipid metabolism, insulin sensitivity, energy homeostasis but also how they modulate mood, cognition and sexual behavior (and plenty of other neurological effects (ARs in the hippocampus and amygdala for example greatly modulate stress-related behaviors)). ARs exists in an inactive state in the cytoplasm, bound to heat shock proteins (HSPs) and other chaperones, which stabilize it until ligand binding occurs. When it comes to the domains of ARs: -The N-terminal domain (NTD) contains activation function 1 (AF1), which is involved in transcriptional activation. It interacts with co-regulatory proteins to modulate gene expression. -The DNA-binding domain (DBD) contains zinc finger motifs that allow the receptor to bind to specific DNA sequences called androgen response elements (AREs) in the promoter regions of target genes. -The hinge region connects the DBD to the ligand-binding domain and contains a nuclear localization signal (NLS) to direct the receptor to the cell nucleus upon activation. -The ligand-binding domain (LBD) is located at the C-terminus, this domain forms a pocket that binds androgens with high specificity and affinity. It also contains activation function 2 (AF2), which is critical for recruiting co-activator proteins after ligand binding. Now chromosomes are structures in the nucleus of cells that carry genetic information in the form of DNA. Each chromosome contains many genes, and we typically have 46 chromosomes (23 pairs), including 22 pairs of autosomes (non-sex chromosomes) and one pair of sex chromosomes (XX for females and XY for males). Males (XY) inherit their single X chromosome (and X-linked genes) from their mother and the Y chromosome from their father. Females (XX): Inherit one X chromosome from each parent. Mitochondrial genes are also inherited solely from the mother, as mitochondria (and their DNA) come from the egg. Why do these matter? Because the AR gene, is located on the X chromosome (Xq11-12). Males, inherit their single AR gene from their mother’s X chromosome. The father contributes the Y chromosome, which lacks AR. Thus, for males, the androgen receptor is exclusively inherited from the mother’s side. Females, inherit one AR allele from the mother and one from the father (via his X chromosome). If these were too complicated here’s a brief summary of how androgen receptors work. A molecule of an androgen hormone slips through the cell’s outer membrane since it’s fat-soluble, it finds the androgen receptor and goes to the ligand-binding domain (LBD) in the cytoplasm. This causes the receptor to change shape and kick off the heat shock proteins (HSPs) in order to expose parts of the receptor that were hidden. Once activated, it travels to the cell’s nucleus with the help of nuclear localization signal (NLS) in order to influence the cell’s instructions (DNA is stored in the nucleus). Once in the nucleus, two activated receptors “team up” (just an analogy for dimerization) to form a “homodimer” which then binds to specific spots on the DNA called androgen response elements (AREs). In order to modulate gene expression, the receptor needs help from other proteins called co-activators or co-repressors that “open up” the DNA (by adding chemical tags to histones, which are like spools that DNA is wrapped around) or “close it off” to control whether genes are turned on or off. They also connect the receptor to the cell’s machinery that reads DNA. Then all these instruct the cell to make specific proteins by turning on or off certain genes, which then carry out the androgen’s effects. In order to understand how we can have healthy ARs and improve their function, we must remember that the activity of ARs is regulated by: -Ligand availability (controlled by enzymes like 5α-reductase and aromatase). -Co-activators such as SRC-1 and CBP/p300. -Co-repressors such as NCoR and SMRT. -Phosphorylation, acetylation and ubiquitination -Feedback mechanisms: Androgen signaling regulates the hypothalamic-pituitary-gonadal axis, controlling testosterone production.

In the latest issue! ErbB family receptor dimerization dynamics and dysregulation via long-term single-molecule imaging dlvr.it/TSnt1T

🔥ErbB receptor dimerization dynamics via long-term single-molecule imaging 🆙 @CellCellPress ☑UCNP-SPT enables tracking of EGFR/HER2/HER3 🎯Oncogenic EGFR muts promote stable ligand-independent dimerization 🎙Dr. Kaibo Ma @OncoAlert @Larvol cell.com/cell/fulltext/S0092…

Our wirk has been accepted in Organic Letters: “Gold(I)-Catalyzed Intermolecular Dimerization of Internal Alkynes: Access to Bis-Indolic trans-Fused Pentacycles with a Central Seven-Membered Ring” We report a gold(I)-catalyzed approach to access complex bis-indolic pentacycles.