13 citations
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November 2012 in “PLoS ONE” A gene mutation in mice causes severe skin disorder similar to a human condition.
May 2005 in “Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature” Truncated LTBP-1 disrupts TGF-beta signaling, affecting hair growth.
26 citations
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February 2021 in “FEBS Journal” Targeting regulatory T cells may help treat age-related diseases.
19 citations
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July 1997 in “British Journal of Dermatology” LHTric-1 is a specific antibody useful for studying hair and nail formation.
3 citations
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January 2022 in “Burns & Trauma” CTHRC1 helps sweat glands recover by rebuilding nearby blood vessels.
TLR2 is crucial for hair growth and regeneration, and boosting it can help prevent hair loss.
July 2017 in “OPAL (Open@LaTrobe) (La Trobe University)” High-throughput LC-MS screening is effective for finding new autotaxin inhibitors for asthma treatment.
5 citations
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May 2024 in “Developmental Cell” Lower GATA3 levels in mice help hair regrow by changing certain immune cells.
555 citations
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July 2001 in “Genes & Development” Tcf3 and Lef1 are key in deciding skin stem cell roles.
1 citations
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May 2023 in “The Journal of Immunology” CD4 T cells can cause alopecia areata by activating CD8 T cells to attack hair follicles.
1 citations
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April 2017 in “Journal of Investigative Dermatology” CCL5 is important for the hair growth potential of human dermal papilla cells.
77 citations
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June 2002 in “Journal of Investigative Dermatology” CD44 variant changes start alopecia areata, but don't maintain it.
Not having the gene PLAAT3 leads to fat loss, high insulin resistance, and abnormal fat levels in the blood due to a disruption in fat cell development and function.
October 2025 in “Science Advances” IFN-γ production by CD4 T cells is crucial for causing alopecia areata.
CCC1 is essential for ion balance and proper plant cell function.
27 citations
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September 1992 in “The Lancet” ICL is a condition with low CD4+ T cells like AIDS but not caused by HIV, and normal CD4+ T cell counts may vary between men and women.
5 citations
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August 2013 in “InTech eBooks” KLF4 is important for maintaining stem cells and has potential in cancer treatment and wound healing.
9 citations
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January 2023 in “International Journal of Biological Sciences” CTHRC1 is essential for healing and preventing heart rupture after a heart attack.
July 2022 in “The journal of investigative dermatology/Journal of investigative dermatology” Thymic stromal lymphopoietin (TSLP) promotes hair growth by stimulating specific skin cells.
43 citations
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September 2014 in “Molecular Plant” CLE40 and CRN/CLV2 pathways have opposite effects on root growth in Arabidopsis.
4 citations
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January 2022 in “The journal of investigative dermatology/Journal of investigative dermatology” A faulty KLHL24 gene leads to hair loss by damaging hair follicle stem cells.
Deleting the MAD2L1 gene in mice led to rapid tumor growth despite chromosomal instability.
42 citations
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June 2019 in “Aging” 3,4,5-tri-O-caffeoylquinic acid promotes hair growth by activating the β-catenin pathway.
November 2025 in “Journal of Investigative Dermatology” TEDAR is crucial for skin cell differentiation and barrier formation.
40 citations
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May 2005 in “Journal of Cell Science” Truncated LTBP-1 disrupts TGF-β signaling, affecting hair growth.
April 2019 in “The journal of investigative dermatology/Journal of investigative dermatology” 848 genes related to fat and metabolism are less active in people with Central Centrifugal Cicatricial Alopecia.
2 citations
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May 2020 in “Journal of the American Academy of Dermatology” Hair shaft changes may be linked to CCCA, but their role is unclear.
September 2025 in “Science Advances” PADI4 enzyme slows down cell growth in developing hair follicles.
November 2023 in “Scientific Reports” A gene mutation in Lama3 is linked to a common type of hair loss.
36 citations
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July 1996 in “The journal of investigative dermatology/Journal of investigative dermatology” Mice with the 'lanceolate hair' mutation have abnormal hair and skin similar to human Netherton's syndrome.