@dorisloh.bsky.social
Proud to announce our bioRxiv preprint: tinyurl.com/2k5a459h
Kudos to co-authors Chuffa, Seiva, and Reiter for demonstrating a universal regulator that restores normal cellular phase behavior—disrupting the condensates cancer cells exploit.
#PhaseSeparation #CancerResearch #Biophysics #Melatonin
Kudos to co-authors Chuffa, Seiva, and Reiter for demonstrating a universal regulator that restores normal cellular phase behavior—disrupting the condensates cancer cells exploit.
#PhaseSeparation #CancerResearch #Biophysics #Melatonin
February 7, 2026 at 2:22 PM
Proud to announce our bioRxiv preprint: tinyurl.com/2k5a459h
Kudos to co-authors Chuffa, Seiva, and Reiter for demonstrating a universal regulator that restores normal cellular phase behavior—disrupting the condensates cancer cells exploit.
#PhaseSeparation #CancerResearch #Biophysics #Melatonin
Kudos to co-authors Chuffa, Seiva, and Reiter for demonstrating a universal regulator that restores normal cellular phase behavior—disrupting the condensates cancer cells exploit.
#PhaseSeparation #CancerResearch #Biophysics #Melatonin
100 mg/kg melatonin achieved better results than 50 mg/kg in suppressing aggressive Ehrlich ascites carcinoma in mice. The question is, how much is a 100 mg/kg mouse dose for a 65kg human?
Answer: 4600 mg (with adjustment for body surface area, metabolic rate, bioavailability, and administration).
Answer: 4600 mg (with adjustment for body surface area, metabolic rate, bioavailability, and administration).
June 17, 2025 at 5:35 PM
100 mg/kg melatonin achieved better results than 50 mg/kg in suppressing aggressive Ehrlich ascites carcinoma in mice. The question is, how much is a 100 mg/kg mouse dose for a 65kg human?
Answer: 4600 mg (with adjustment for body surface area, metabolic rate, bioavailability, and administration).
Answer: 4600 mg (with adjustment for body surface area, metabolic rate, bioavailability, and administration).
Why do cancer cells develop resistance to chemo drugs like doxorubicin?
Doxorubicin interacts with the tumor suppressor gene p53 (wildtype and mutants) to cause phase separation and accelerated aggregation, leading to increased survival and proliferation.
pubmed.ncbi.nlm.nih.gov/38435052/
Doxorubicin interacts with the tumor suppressor gene p53 (wildtype and mutants) to cause phase separation and accelerated aggregation, leading to increased survival and proliferation.
pubmed.ncbi.nlm.nih.gov/38435052/
May 27, 2025 at 2:45 PM
Why do cancer cells develop resistance to chemo drugs like doxorubicin?
Doxorubicin interacts with the tumor suppressor gene p53 (wildtype and mutants) to cause phase separation and accelerated aggregation, leading to increased survival and proliferation.
pubmed.ncbi.nlm.nih.gov/38435052/
Doxorubicin interacts with the tumor suppressor gene p53 (wildtype and mutants) to cause phase separation and accelerated aggregation, leading to increased survival and proliferation.
pubmed.ncbi.nlm.nih.gov/38435052/
Worried about your pathogenic SNPs? Peer-reviewed 2025 paper shows how phase separation mediates non-coding SNP interactions with their target genes. When the transcription factor RUNX2 phase separates, it can recruit SNP rs4683184, associated with osteoporosis, to increase osteoblast production.
RUNX2 Phase Separation Mediates Long‐Range Regulation Between Osteoporosis‐Susceptibility Variant and XCR1 to Promote Osteoblast Differentiation
A GWAS intergenic SNP (rs4683184) acts as an enhancer, altering the binding affinity of the transcription factor RUNX2 and resulting in changes in XCR1 expression and osteoblast differentiation. RUNX....
advanced.onlinelibrary.wiley.com
April 21, 2025 at 2:11 PM
Worried about your pathogenic SNPs? Peer-reviewed 2025 paper shows how phase separation mediates non-coding SNP interactions with their target genes. When the transcription factor RUNX2 phase separates, it can recruit SNP rs4683184, associated with osteoporosis, to increase osteoblast production.
ATP is biphasic: low levels promote & high levels inhibit protein aggregation. Novel discovery shows a-Syn amyloids fully degrade ATP at normal cellular concentrations (2 mM), using it to stabilize pathological aggregations. tinyurl.com/e7626sc4 Melatonin complexes with ATP to inhibit aggregation.
April 9, 2025 at 6:43 PM
ATP is biphasic: low levels promote & high levels inhibit protein aggregation. Novel discovery shows a-Syn amyloids fully degrade ATP at normal cellular concentrations (2 mM), using it to stabilize pathological aggregations. tinyurl.com/e7626sc4 Melatonin complexes with ATP to inhibit aggregation.