BFT - Research Technician for Dermatology
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Job Summary
Location: 149 13th St, Charlestown, MA 02129Start Date: July 1st 2026, 40 hours a week
Qualifications
BFT position in Dermatology available at Massachusetts General Hospital/Harvard Medical School
Dermatology, Cutaneous Biology Research Center
PI: Alexander G. Marneros, MD/PhD
Project: “Novel Mechanisms in Skin Inflammation”.
Research Overview
My laboratory investigates how disrupted epithelial differentiation, inflammation, and wound-repair responses drive genetic skin disease and age-related disorders. We combine human genetics, mouse models, multi-omics, and functional studies to uncover disease mechanisms and translate those discoveries into new therapeutic strategies. Our work is highly interdisciplinary, disease-focused, and supported by four major NIH-funded research programs. Although rooted in dermatology and wound healing, our discoveries have also advanced understanding in kidney disease, fibrosis, macrophage biology, angiogenesis, and neovascular age-related macular degeneration.
Research Program I
Keratinocyte–immune cell interactions in cutaneous inflammation
Skin inflammation is shaped not only by immune cells, but also by intrinsic abnormalities in keratinocytes. We study the earliest pathogenic events that initiate inflammatory skin disease, with the goal of identifying interventions that can block inflammation before it becomes chronic. Our work showed that impaired keratinocyte differentiation can be an initiating event in cutaneous inflammation. In particular, we identified AP-2α as a key regulator of the transition from keratinocyte proliferation to terminal differentiation. Loss of this pathway drives keratinocyte hyperproliferation, defective differentiation, and inflammatory changes that resemble psoriasis. We further discovered that AP-2 activity is controlled by KCTD1/KCTD15 complexes, linking epithelial differentiation to inflammatory disease and skin appendage development. These findings highlight keratinocytes as active drivers of inflammation and suggest new therapeutic strategies aimed at restoring epithelial homeostasis.
Research Program II
From wound healing to epithelial differentiation, developmental signaling, and fibrosis
A central theme of our research is that clinical observation can lead to fundamental biological discovery. Our studies of aplasia cutis congenita (ACC), a congenital scalp defect, uncovered the first genetic causes of this disorder and transformed understanding of how epithelial tissues develop and are maintained. We identified pathogenic mutations in BMS1 and KCTD1, then used these discoveries to define molecular pathways that regulate epithelial differentiation in both skin and kidney. Our work revealed a critical AP-2β/KCTD1 axis required for distal convoluted tubule differentiation and maintenance, and showed that loss of this pathway causes inflammation, fibrosis, and renal dysfunction. We also discovered that ACC is not caused by a primary keratinocyte defect, but instead arises from abnormal cranial neural crest–derived mesenchyme that fails to support formation of the overlying epidermis. This revealed a new mesenchymal-to-epithelial inductive signaling mechanism in scalp development. Together, these studies show how rare disease genetics can uncover broadly important principles of development, tissue homeostasis, and fibrosis.
To apply, please send (1) cover letter highlighting past research experience, your research interests and career goals, (2) CV and (3) the contact info of references via email to Alexander Marneros, MD/PhD, Associate Professor, Harvard Medical School, Massachusetts General Hospital at [email protected]
Additional Job Details (if applicable)
Education: Bachelors Degree
Experience: Some lab experience preferred, helpful if had experience with mice
Remote Type
Work Location
Scheduled Weekly Hours
Employee Type
Work Shift
Pay Range
$20.16 - $29.01/Hourly
Grade
5
EEO Statement:
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