Farah Lubin

Last updated
Farah D. Lubin
Flubin.tif
Born
Haiti
NationalityAmerican
Alma mater Alabama State University
Binghamton University
Baylor College of Medicine
Known forRole of epigenetic modifications in memory
Awards2022 Commission on the Status of Women Padma Award, Becky Trigg Outstanding UAB Faculty Member, 2020 Dean's Excellence Award Winner in Diversity, 2020 President's Champion Award for Diversity, 2017 Dean’s Excellence in Mentorship Award, 2008 FASEB Professional Development and Enrichment Award
Scientific career
FieldsNeuroscience, epigenetics
Institutions University of Alabama Birmingham

Farah D. Lubin is an American neuroscientist and Professor of Neurobiology and Cell, Developmental, and Integrative Biology at the University of Alabama at Birmingham within the Heersink School of Medicine. Lubin is the Principal Investigator of the Lubin Lab which explores the epigenetic mechanisms underlying cognition and how these mechanisms are altered in disease states such as epilepsy and neurodegeneration. Lubin discovered the role of NF-κB in fear memory reconsolidation and also uncovered a novel role for epigenetic regulation of BDNF during long-term memory formation and in epilepsy leading to memory loss. Lubin is a champion for diversity at UAB as the Director of the Roadmap Scholar Program and as a faculty mentor for several institutional and national programs to increase retention of underrepresented minorities in STEM.

Contents

Early life and education

Lubin grew up in New York and attended high school in New York City. [1] While in high school, she worked as a nursing assistant in New York City during the height of the HIV/AIDS epidemic. [2] At the time she had a desire to pursue a career in medicine, but her experience in the clinic showed her that academia and science are where cures are discovered. [2] Before completing high school, Lubin toured many American Historically Black Colleges and Universities and became acutely aware of the barriers to career success due to her identity as a Black woman in science. [2] Motivated to overcome these barriers, Lubin pursued her undergraduate degree at Alabama State University in 1992. [2] She received a full scholarship and participated in the National Institutes of Health sponsored Minority Biomedical Research Support Program. [2] Her summer research experience at the Memorial Sloan Kettering Cancer Center in New York City highlighted her passion for scientific discovery and she chose to pursue a career and academia. [2]

In 1996, Lubin obtained her Bachelors of Science in biology with a Minor in Chemistry from Alabama State University, graduating summa cum laude with honors for her senior research thesis in the lab of Eddie Moore. [1] Lubin then returned to New York State to join the Cell and Molecular Biology Graduate Program at Binghamton University (SUNY). [3] She trained under the mentorship of Dennis W. McGee exploring cytokine signalling in epithelial cells. [4] Lubin inhibited integrin signalling in epithelial cells and exposed them to proinflammatory cytokines. [4] She found that a3B1 integrin signalling may be responsible for suppression of cytokine responses in epithelial cells during inflammation and wound healing. [4]

After completing her graduate training in 2001, Lubin pursued postdoctoral training at Baylor College of Medicine in the Texas Children's Hospital under the mentorship of Anne E. Anderson. [5] Lubin explored how glutamate signalling is coupled to nuclear factor-kappa B expression and transcriptional regulation in the hippocampus. [6] She found that kainate, a glutamate analog, elicited activation of NF-κB via the classical IkB kinase pathway and both ERK and PI3K were implicated in regulation of transcription via NF-κB in hippocampal area CA3. [6]

In 2006, Lubin pursued further postdoctoral training in the lab of David Sweatt at Baylor College of Medicine. [1] Lubin moved with the lab to the University of Alabama at Birmingham and continued her postdoctoral training there. [1] During this second phase of her postdoctoral training, Lubin explored epigenetic transcriptional regulation of fear memory reconsolidation. [7] She found that fear memory retrieval activates the NK-kB signalling pathway and leads to epigenetic modifications of the gene promoters in the hippocampus via IKKa-mediated mechanisms. [7] Lubin then discovered a role for epigenetic modifications of the bdnf gene in fear memory consolidation. [8] She found that bdnf DNA methylation altered bdnf transcription and that blocking BDNF expression in the hippocampus resulted in impaired fear memory consolidation. [8] Upon completion of her postdoctoral fellowship, Lubin became one of the first UAB scientists to obtain a K99 NIH grant to support her transition into her independent career. [1]

Career and research

In 2009, Lubin became an Assistant Professor of Neurobiology at the University of Alabama at Birmingham as well as an Investigator in the Evelyn McKnight Brain Institute and an assistant professor in the Department of Cell Biology. [3] She was then promoted to Associate Professor and now holds appointments in the Comprehensive Center for Healthy Aging, the Comprehensive Neuroscience Center, the Center for Glial Biology and Medicine, the Center for Neurodegeneration and Experimental Therapeutics, the Civitan International Research Center, and the Center for Craniofacial, Oral, and Dental Disorders. [3] Lubin is also actively involved in recruitment as well as continued support of the academic and medical trainees at UAB. [9] In 2017, Lubin became co-director of Research Training for the NIH/NINDS Mentored Experiences in Research Instruction, and Teaching (MERIT) Program which supports postdoctoral fellows at UAB in achieving their career goals. [10] Lubin also serves on the admissions committee for the graduate program in Neuroscience and is a member of the advisory board for the Medical Scientists Training Program. [9]

Lubin is also the Principal Investigator of the Lubin Lab where she leads a research program centered around exploring the molecular and cellular mechanisms of epigenetic modifications that mediate cognition and that become aberrant in disease processes such as epilepsy and memory disorders. [11] She has found that transcription implicated in memory formation is tightly regulated by DNA methylation in the hippocampus. [11]

Histone methylation in memory consolidation

Lubin is a pioneer in the study of histone modifications in cognition. Early in her independent career she explored the role of histone methylation in memory formation. [12] She found that histone methylation is actively regulated in the adult hippocampus and that methylation is required for the long-term consolidation of fear memories. [12] In 2012, Lubin and her team discovered the critical role for GLP lysine dimethyltransferase complex mediated lysination and methylation in both the hippocampus and the entorhinal cortex during memory consolidation. [12]

Histone hydroxymethylation in memory consolidation

Lubin and her group then explored the role of epigenetic methylation in the retrieval of memories. She found that retrieval of fear memories increased the levels of H3K4me and 5hmC methylation in the dorsal hippocampus. [13] Her findings supported the link between methylation and hydroxymethylation in gene transcription associated with memory retrieval in the hippocampus. [13]

Memory loss in epilepsy

In 2015, Lubin and her team discovered a role for DNA methylation in the memory loss associated with epilepsy. [14] They detected aberrant DNA methylation patterns at the bdnf gene in rat models of epilepsy and investigated how these might be impacting memory formation. [14] They found that epilepsy decreased DNA methylation of the bdnf gene leading to increased levels of BDNF which impaired memory consolidation. [14] When they artificially increased the methylation at the bdnf gene, this led to improvements in memory in epileptic animals. [14]

Advocacy

Lubin is a fervent advocate for diversity in STEM and has dedicated herself to enhancing diversity and opportunities for underrepresented minority students to excel in STEM at the University of Alabama. [9] In 2014, Lubin helped to establish the NIH/NINDS Roadmap Scholar Program for graduate students in neuroscience at UAB. [15] Lubin is now the co-director of the program. [16] In this role, Lubin oversees and coordinates graduate student mentoring, social and networking events, workshops and other initiatives to support underrepresented graduate students in neuroscience. [17] She serves as a faculty mentor in the program to guide students to career success in neuroscience and she also co-organizes the yearly NEURAL Conference to bring together underrepresented minority students from across the country to share their research and scientific accomplishments. [9] Lubin is also a mentor for the UAB Society for Advancement of Chicanos/Hispanics and Native Americans in Science Chapter. [9] Her support of underrepresented junior faculty and postdoctoral fellows at UAB is felt through her involvement in the Health Disparities Research Education Program as a Grant Reviewer. [18]

Awards and honors

Select publications

Related Research Articles

<span class="mw-page-title-main">Epigenetics</span> Study of DNA modifications that do not change its sequence

In biology, epigenetics is the study of heritable traits, or a stable change of cell function, that happen without changes to the DNA sequence. The Greek prefix epi- in epigenetics implies features that are "on top of" or "in addition to" the traditional genetic mechanism of inheritance. Epigenetics usually involves a change that is not erased by cell division, and affects the regulation of gene expression. Such effects on cellular and physiological phenotypic traits may result from environmental factors, or be part of normal development. They can lead to cancer.

<span class="mw-page-title-main">Fear conditioning</span> Behavioral paradigm in which organisms learn to predict aversive events

Pavlovian fear conditioning is a behavioral paradigm in which organisms learn to predict aversive events. It is a form of learning in which an aversive stimulus is associated with a particular neutral context or neutral stimulus, resulting in the expression of fear responses to the originally neutral stimulus or context. This can be done by pairing the neutral stimulus with an aversive stimulus. Eventually, the neutral stimulus alone can elicit the state of fear. In the vocabulary of classical conditioning, the neutral stimulus or context is the "conditional stimulus" (CS), the aversive stimulus is the "unconditional stimulus" (US), and the fear is the "conditional response" (CR).

<span class="mw-page-title-main">Regulation of gene expression</span> Modifying mechanisms used by cells to increase or decrease the production of specific gene products

Regulation of gene expression, or gene regulation, includes a wide range of mechanisms that are used by cells to increase or decrease the production of specific gene products. Sophisticated programs of gene expression are widely observed in biology, for example to trigger developmental pathways, respond to environmental stimuli, or adapt to new food sources. Virtually any step of gene expression can be modulated, from transcriptional initiation, to RNA processing, and to the post-translational modification of a protein. Often, one gene regulator controls another, and so on, in a gene regulatory network.

In biology, reprogramming refers to erasure and remodeling of epigenetic marks, such as DNA methylation, during mammalian development or in cell culture. Such control is also often associated with alternative covalent modifications of histones.

Histone methylation is a process by which methyl groups are transferred to amino acids of histone proteins that make up nucleosomes, which the DNA double helix wraps around to form chromosomes. Methylation of histones can either increase or decrease transcription of genes, depending on which amino acids in the histones are methylated, and how many methyl groups are attached. Methylation events that weaken chemical attractions between histone tails and DNA increase transcription because they enable the DNA to uncoil from nucleosomes so that transcription factor proteins and RNA polymerase can access the DNA. This process is critical for the regulation of gene expression that allows different cells to express different genes.

<span class="mw-page-title-main">DNA demethylation</span> Removal of a methyl group from one or more nucleotides within a DNA molecule.

For molecular biology in mammals, DNA demethylation causes replacement of 5-methylcytosine (5mC) in a DNA sequence by cytosine (C). DNA demethylation can occur by an active process at the site of a 5mC in a DNA sequence or, in replicating cells, by preventing addition of methyl groups to DNA so that the replicated DNA will largely have cytosine in the DNA sequence.

Memory consolidation is a category of processes that stabilize a memory trace after its initial acquisition. A memory trace is a change in the nervous system caused by memorizing something. Consolidation is distinguished into two specific processes. The first, synaptic consolidation, which is thought to correspond to late-phase long-term potentiation, occurs on a small scale in the synaptic connections and neural circuits within the first few hours after learning. The second process is systems consolidation, occurring on a much larger scale in the brain, rendering hippocampus-dependent memories independent of the hippocampus over a period of weeks to years. Recently, a third process has become the focus of research, reconsolidation, in which previously consolidated memories can be made labile again through reactivation of the memory trace.

<span class="mw-page-title-main">8-Oxo-2'-deoxyguanosine</span> Chemical compound

8-Oxo-2'-deoxyguanosine (8-oxo-dG) is an oxidized derivative of deoxyguanosine. 8-Oxo-dG is one of the major products of DNA oxidation. Concentrations of 8-oxo-dG within a cell are a measurement of oxidative stress.

<span class="mw-page-title-main">Memory</span> Faculty of mind to store and retrieve data

Memory is the faculty of the mind by which data or information is encoded, stored, and retrieved when needed. It is the retention of information over time for the purpose of influencing future action. If past events could not be remembered, it would be impossible for language, relationships, or personal identity to develop. Memory loss is usually described as forgetfulness or amnesia.

While the cellular and molecular mechanisms of learning and memory have long been a central focus of neuroscience, it is only in recent years that attention has turned to the epigenetic mechanisms behind the dynamic changes in gene transcription responsible for memory formation and maintenance. Epigenetic gene regulation often involves the physical marking of DNA or associated proteins to cause or allow long-lasting changes in gene activity. Epigenetic mechanisms such as DNA methylation and histone modifications have been shown to play an important role in learning and memory.

Behavioral epigenetics is the field of study examining the role of epigenetics in shaping animal and human behavior. It seeks to explain how nurture shapes nature, where nature refers to biological heredity and nurture refers to virtually everything that occurs during the life-span. Behavioral epigenetics attempts to provide a framework for understanding how the expression of genes is influenced by experiences and the environment to produce individual differences in behaviour, cognition, personality, and mental health.

The epigenetics of schizophrenia is the study of how inherited epigenetic changes are regulated and modified by the environment and external factors and how these changes influence the onset and development of, and vulnerability to, schizophrenia. Epigenetics concerns the heritability of those changes, too. Schizophrenia is a debilitating and often misunderstood disorder that affects up to 1% of the world's population. Although schizophrenia is a heavily studied disorder, it has remained largely impervious to scientific understanding; epigenetics offers a new avenue for research, understanding, and treatment.

Epigenetic regulation of neurogenesis is the role that epigenetics plays in the regulation of neurogenesis.

Epigenetics of physical exercise is the study of epigenetic modifications to the cell genome resulting from physical exercise. Environmental factors, including physical exercise, have been shown to have a beneficial influence on epigenetic modifications. Generally, it has been shown that acute and long-term exercise has a significant effect on DNA methylation, an important aspect of epigenetic modifications.

Epigenetics of depression is the study of how epigenetics contribute to depression.

Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more. These changes can lead to transgenerational stress inheritance.

<span class="mw-page-title-main">Epigenetic priming</span> Type of modification to a cells epigenome

Epigenetic priming is the modification to a cell's epigenome whereby specific chromatin domains within a cell are converted from a closed state to an open state, usually as the result of an external biological trigger or pathway, allowing for DNA access by transcription factors or other modification mechanisms. The action of epigenetic priming for a certain region of DNA dictates how other gene regulation mechanisms will be able to act on the DNA later in the cell’s life. Epigenetic priming has been chiefly investigated in neuroscience and cancer research, as it has been found to play a key role in memory formation within neurons and tumor-suppressor gene activation in cancer treatment respectively.

<span class="mw-page-title-main">Courtney A. Miller</span> American neuroscientist, researcher

Courtney A. Miller is an American neuroscientist and Professor of the Department of Molecular Medicine at the Scripps Research Institute in Jupiter, Florida. Miller investigates the biological basis of neurological and neuropsychiatric diseases and develops novel therapeutics based on her mechanistic discoveries.

<span class="mw-page-title-main">Johannes Gräff</span> Swiss neuroscientist

Johannes Gräff is a Swiss neuroscientist. He currently works as an Associate Professor at the École Polytechnique Fédérale de Lausanne (EPFL). His research focuses on the neuroepigenetic bases of physiological and pathological memory formation.

Epigenetics of bipolar disorder is the effect that epigenetics has on triggering and maintaining bipolar disorder.

References

  1. 1 2 3 4 5 "Happy Holidays from the CIVITAN INTERNATIONAL RESEARCH CENTER" (PDF). UAB.edu. 2019. Retrieved June 3, 2020.
  2. 1 2 3 4 5 6 Windsor, Matt (December 9, 2019). "'I was tired of being the only': words and deeds that can save science careers" (PDF). UAB.edu. Retrieved June 3, 2020.
  3. 1 2 3 "UASOM Faculty Profiles". apps.medicine.uab.edu. Retrieved 2020-06-04.
  4. 1 2 3 Lubin, Farah D.; Segal, Miriam; Mcgee, Dennis W. (2003). "Regulation of epithelial cell cytokine responses by the α3β1 integrin". Immunology. 108 (2): 204–210. doi:10.1046/j.1365-2567.2003.01577.x. ISSN   1365-2567. PMC   1782878 . PMID   12562329.
  5. ↑ "Neurotree - Farah Lubin". neurotree.org. Retrieved 2020-06-04.
  6. 1 2 Lubin, F. D.; Johnston, L. D.; Sweatt, J. D.; Anderson, A. E. (2005-01-01). "Kainate mediates nuclear factor-kappa B activation in hippocampus via phosphatidylinositol-3 kinase and extracellular signal-regulated protein kinase". Neuroscience. 133 (4): 969–981. doi:10.1016/j.neuroscience.2005.03.028. ISSN   0306-4522. PMID   15916859. S2CID   20541675.
  7. 1 2 Lubin, Farah D.; Sweatt, J. David (2007-09-20). "The IκB Kinase Regulates Chromatin Structure during Reconsolidation of Conditioned Fear Memories". Neuron. 55 (6): 942–957. doi:10.1016/j.neuron.2007.07.039. ISSN   0896-6273. PMC   2587178 . PMID   17880897.
  8. 1 2 Lubin, Farah D.; Roth, Tania L.; Sweatt, J. David (2008-10-15). "Epigenetic Regulation of bdnf Gene Transcription in the Consolidation of Fear Memory". Journal of Neuroscience. 28 (42): 10576–10586. doi:10.1523/JNEUROSCI.1786-08.2008. ISSN   0270-6474. PMC   3312036 . PMID   18923034.
  9. 1 2 3 4 5 6 7 Canevaro, Mary Ashley. "Lubin named 2020 Dean's Excellence Award Winner in Diversity - School of Medicine - News". UAB Medicine News. Retrieved 2020-06-04.
  10. ↑ Armbrester, Jami K. "MERIT Leadership - MERIT Program | UAB". www.uab.edu. Retrieved 2020-06-04.
  11. 1 2 "Lubin Lab at UAB – Department of Neurobiology at the University of Alabama at Birmingham, Evelyn F. McKnight Brain Institute" . Retrieved 2020-06-04.
  12. 1 2 3 Gupta, Swati; Kim, Se Y.; Artis, Sonja; Molfese, David L.; Schumacher, Armin; Sweatt, J. David; Paylor, Richard E.; Lubin, Farah D. (2010-03-10). "Histone Methylation Regulates Memory Formation". Journal of Neuroscience. 30 (10): 3589–3599. doi: 10.1523/JNEUROSCI.3732-09.2010 . ISSN   0270-6474. PMC   2859898 . PMID   20219993.
  13. 1 2 Webb, William M.; Sanchez, Richard G.; Perez, Gabriella; Butler, Anderson A.; Hauser, Rebecca M.; Rich, Megan C.; O'Bierne, Aidan L.; Jarome, Timothy J.; Lubin, Farah D. (2017-07-01). "Dynamic association of epigenetic H3K4me3 and DNA 5hmC marks in the dorsal hippocampus and anterior cingulate cortex following reactivation of a fear memory". Neurobiology of Learning and Memory. Memory reconsolidation and memory updating. 142 (Pt A): 66–78. doi:10.1016/j.nlm.2017.02.010. ISSN   1074-7427. PMID   28232238. S2CID   4353959.
  14. 1 2 3 4 Parrish, R. Ryley; Buckingham, Susan C.; Mascia, Katherine L.; Johnson, Jarvis J.; Matyjasik, Michal M.; Lockhart, Roxanne M.; Lubin, Farah D. (2015). "Methionine increases BDNF DNA methylation and improves memory in epilepsy". Annals of Clinical and Translational Neurology. 2 (4): 401–416. doi:10.1002/acn3.183. ISSN   2328-9503. PMC   4402085 . PMID   25909085.
  15. ↑ "UAB launches roadmap for underrepresented grad students interested in neuroscience - News". UAB News. Retrieved 2020-06-04.
  16. ↑ White, Jamie. "Career Coaches - Neuroscience Roadmap Scholars Program | UAB". www.uab.edu. Retrieved 2020-06-04.
  17. ↑ Furgeson, Tyler. "Home - Neuroscience Roadmap Scholars Program | UAB". www.uab.edu. Retrieved 2020-06-04.
  18. ↑ "Junior Faculty & Post Doctoral - School of Medicine - Minority Health & Health Disparities Research Center | UAB". www.uab.edu. Retrieved 2020-06-04.
  19. ↑ School, UAB Graduate. "Congratulations to UAB's Excellent Faculty Mentors on 2017 Award - Graduate School | UAB". www.uab.edu. Retrieved 2020-06-04.
  20. ↑ "Health Services Foundation awards granted to UAB researchers - News". UAB News. Retrieved 2020-06-04.
  21. ↑ admin. "Dr. Farah Lubin: Impacting Lives at the Civitan International Research Center | Civitan International". Archived from the original on 2020-06-04. Retrieved 2020-06-04.
  22. ↑ "FASEB MARC PROGRAM ANNOUNCES THE RECIPIENTS OF THE 2008 POSTDOCTORAL PROFESSIONAL DEVELOPMENT AND ENRICHMENT AWARD" (PDF). faseb.org. 2008. Archived from the original (PDF) on July 8, 2021. Retrieved June 3, 2020.
  23. ↑ "American Epilepsy Society Relationships 2004 Annual report" (PDF). aesnet.org. 2004. Archived from the original (PDF) on June 18, 2015. Retrieved June 3, 2020.
  24. 1 2 3 4 5 6 7 8 9 10 11 12 "Farah Lubin - Publications". neurotree.org. Retrieved 2020-06-04.
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