11 citations
,
February 2018 in “Oncotarget” Lower SMAD2/3 activation predicts more severe skin cancer.
April 2017 in “Journal of Investigative Dermatology” The BMP/Smads pathway and Id2 gene control hair follicle stem cells, affecting their rest and growth phases.
3 citations
,
July 2022 in “Brain and Behavior” The HtrA1L364P mutation causes brain dysfunction and blood vessel damage.
SMAD4 is crucial for muscle repair in young adults but not in aged mice.
111 citations
,
June 2002 in “The EMBO Journal” Too much Smad7 can cause serious changes in skin tissues, including problems with hair growth, thymus shrinkage, and eye development issues.
June 2008 in “The Knowledge Bank (The Ohio State University)” Smad2 and Smad3 are essential for normal skin development, and their absence causes severe skin issues and cancer.
1 citations
,
April 2022 in “Cell Death Discovery” Increasing Smurf2 hinders hair follicle stem cell differentiation and wound healing.
April 2026 in “International Journal of Molecular Sciences” Targeting non-Smad pathways in TGF-β signaling may improve keloid treatment.
12 citations
,
September 2007 in “Wound repair and regeneration” Smad2/3-dependent TGF-β signaling increases during wound healing.
288 citations
,
January 2001 in “Journal of Biological Chemistry” Tgm2 helps stabilize dying cells and aids fibroblast attachment to the extracellular matrix.
Smad4 is crucial for muscle repair, especially in aging, by promoting cell growth over differentiation.
59 citations
,
March 2008 in “The journal of investigative dermatology/Journal of investigative dermatology” Smad-4 and Smad-7 are key in hair follicle development, with other Smads being less important.
April 2019 in “Journal of Investigative Dermatology” Non-coding RNA boosts retinoic acid production and signaling, aiding regeneration.
23 citations
,
May 2023 in “Cell Proliferation” TGF-β and FGF pathways are crucial for skin development and regeneration.
8 citations
,
September 2017 in “Scientific Reports” MAD2B slows down the growth of skin cells that are important for hair development by interacting with TCF4.
31 citations
,
September 2013 in “Stem Cells” Smad1 and Smad5 are essential for hair follicle development and stem cell sleepiness.
321 citations
,
January 2012 in “Cell stem cell” TGF-β2 helps activate hair follicle stem cells by counteracting BMP signals.
14 citations
,
April 2008 in “PROTEOMICS” Increased 14-3-3 proteins may block hair cycle regression, causing hair loss.
September 2025 in “Stem Cell Research & Therapy” TAZ boosts fat cell formation in goat stem cells by activating a specific signaling pathway.
39 citations
,
March 2008 in “Journal of biological chemistry/The Journal of biological chemistry” GLI2 increases follistatin production in human skin cells.
February 2024 in “Planta” TRM21 helps control flavonoid production and root hair growth in Arabidopsis thaliana.
28 citations
,
July 2008 in “Developmental Biology” Smad4 is important for healthy hair follicles because it helps produce a protein needed for hair to stick together and grow.
April 2024 in “bioRxiv (Cold Spring Harbor Laboratory)” A gene network led by RSL4 is crucial for early root hair growth in response to cold in Arabidopsis thaliana.
Deleting the MAD2L1 gene in mice led to rapid tumor growth despite chromosomal instability.
82 citations
,
February 2017 in “Cold Spring Harbor Perspectives in Biology” The TGF-β family helps control how cells change and move, affecting skin, hair, and organ development.
June 2003 in “Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature” GLABRA2 represses root hair formation by inhibiting a specific gene.
Deleting Smad4 and PTEN genes in mice causes rapid, invasive forestomach cancer.
15 citations
,
December 2014 in “PLoS ONE” A mutation in the iRhom2 gene causes hairless mice due to abnormal hair follicle development.
Deleting Smad4 and PTEN genes in mice causes rapid, invasive stomach cancer.
13 citations
,
June 2014 in “Molecular therapy” The lentiviral array can monitor and predict gene activity during stem cell differentiation.