January 2025 in “Cell Communication and Signaling” CXXC5 can both suppress and promote cancer, making it a complex target for treatment.
48 citations
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March 2007 in “The journal of investigative dermatology/Journal of investigative dermatology” Retinoic acid production and signaling in hair follicles are regulated by location and timing, affecting hair growth and cycling.
The balance between cell renewal and differentiation controls the growth of cancerous cells in mouse skin.
January 2026 in “PLoS Biology” ARHGEF3 is essential for proper hair follicle development in mice.
February 2020 in “Definitions” 5 Alpha-Reductase Inhibitors reduce the effects of testosterone by blocking its conversion into a stronger form.
139 citations
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August 2006 in “Molecular and Cellular Biology” Rac1 is vital for hair follicle health but not needed for skin maintenance.
10 citations
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August 1998 in “Journal of Investigative Dermatology” February 2026 in “Toxicology Letters” MK-0773 is a moderate inhibitor of the SRD5A2 enzyme.
4 citations
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June 2024 in “The Kaohsiung Journal of Medical Sciences” Atg5 can promote tumors when autophagy is deficient but suppresses them under normal conditions.
44 citations
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May 2023 in “MedComm” PROTAC technology shows promise for cancer treatment but needs more effective E3 ligase recruiters.
September 2022 in “Research Square (Research Square)” Increasing Rps14 helps grow more inner ear cells and repair hearing cells in baby mice.
124 citations
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September 1992 in “Endocrinology” The human type II 5α-reductase gene, linked to certain male health conditions, has a specific structure and low similarity to other related genes.
2 citations
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December 2004 in “PubMed”
2 citations
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June 2024 in “Frontiers in Plant Science” LLPS is crucial for RALF signaling, aiding plant growth and stress resilience.
2 citations
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January 2023 in “PubMed” Targeting FGF5 could help treat prostate cancer.
1 citations
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November 2024 in “Archives of Dermatological Research” ANE syndrome is caused by a mutation in the RBM28 protein that disrupts ribosome assembly.
October 2016 in “Letters in Drug Design & Discovery” September 2019 in “The journal of investigative dermatology/Journal of investigative dermatology” New RIPK4 gene mutations were found to cause a type of skin and limb birth defect.
39 citations
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February 2011 in “The Prostate/The prostate” Some men's prostate tissues have low enzyme levels due to genetic changes, possibly affecting treatment for prostate enlargement.
26 citations
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September 2005 in “Pharmacology Biochemistry and Behavior” 5alpha-reductase 2 is crucial for proper male brain development and sexual differentiation.
2 citations
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November 2018 in “Indian Journal of Pharmaceutical Education” The developed model can predict effective 5-alpha-reductase enzyme inhibitors.
24 citations
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September 2005 in “Journal of Cellular Biochemistry” Retinoids increase steroid sulfatase activity in leukemia cells through RARα/RXR and involves certain pathways like phosphoinositide 3-kinase and ERK-MAP kinase.
75 citations
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July 2016 in “New phytologist” The protein RSL4 is crucial for making root hairs longer by controlling genes related to cell growth.
14 citations
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April 2024 in “The Journal of Steroid Biochemistry and Molecular Biology” 5α-reductases increase epitestosterone's effect on androgen receptors.
April 2016 in “The journal of investigative dermatology/Journal of investigative dermatology” RPGRIP1L helps skin cells stick together by blocking PKCβII, which can prevent skin blistering like in pemphigus.
127 citations
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July 2002 in “EMBO journal” Normal skin cell renewal doesn't need RAR signaling, but vitamin A-related skin thickening does.
15 citations
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December 2014 in “PLoS ONE” A mutation in the iRhom2 gene causes hairless mice due to abnormal hair follicle development.
January 2026 in “British Journal of Dermatology” ELF5 is essential for skin cell growth and maintenance.
16 citations
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November 1994 in “Developmental Biology” Retinoic acid causes gland formation instead of hair in mouse skin by altering epidermal and dermal interactions.