Philip Beachy | |
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Born | Philip Arden Beachy October 25, 1958 Red Lake, Ontario, Canada |
Alma mater | |
Known for | Hedgehog signaling pathway [1] |
Awards | NAS Award in Molecular Biology (1998) March of Dimes Prize in Developmental Biology (2008) Keio Medical Science Prize (2011) |
Scientific career | |
Fields | Biochemistry |
Institutions | |
Thesis | The UBX Domain in the Bithorax Complex of Drosophila (1986) |
Doctoral advisor | David Hogness [2] |
Website |
Philip Arden Beachy (born October 25, 1958) [3] is Ernest and Amelia Gallo Professor at Stanford University School of Medicine in Palo Alto, California and an Associate at Stanford's Institute of Stem Cell Biology and Regenerative Medicine. [2] [4] [5]
Beachy was born in Red Lake, Ontario, Canada, on October 25, 1958. [6] Beachy spent eight of his early years of life in the hills of central Puerto Rico. His father was a pastor of a rural church. He attended a school taught in Spanish during the day and then learned to read and write English once he came home from school. At nine, Beachy and his family returned to their home base of Goshen, Indiana where he began attending public school. At the early age of 16, Beachy headed off to Goshen College which was very close to home. At this time, Beachy still did not know of his love for science. “Unlike many people who knew they were going to be scientists from a very early age, I didn't decide that I would try to become a scientist until fairly late on in college,” he says. [2]
Beachy received his bachelor's degree in natural sciences at Goshen College. Beachy first envisioned himself as a doctor, but after his first year of college, he decided against pursuing that career. He then decided to focus on biological research. He became interested in this field after reading a serialized form of Horace Freeland Judson's book, The Eighth Day of Creation in The New Yorker. "Reading those articles got me excited about molecular biology," says Beachy. After graduating, he decided to take chemistry courses and do more research at the nearby South Bend campus of Indiana University. A year later, he decided to attend graduate school at Stanford University. There, he studied the molecular genetics behind fruit fly development with David Hogness. [2] [5] Beachy earned his Ph.D in biochemistry in 1986 at Stanford for research into the UBX protein domain.
After receiving his Ph.D, he began working at the Carnegie Institution's Department of Embryology in Baltimore for two years. After his short time there, he accepted a faculty position at the Johns Hopkins University School of Medicine. Beachy began focusing on the Drosophila hedgehog gene, for which he's known for, in 1990. The gene's name originated because fly embryos look spikey if the hedgehog gene is faulty or mutated. The hedgehog gene's main function is to create protein signals in specific cells. These signals, in turn, allow for the formation of embryonic tissues. They do this by instructing neighboring cells to become a certain type of differentiated cell or to simply divide. In other words, this gene is responsible for the development of the appendages and body segments in Drosophila or fruit flies. Humans and other invertebrates have hedgehog genes that behave slightly different than the same gene in the fruit fly. In vertebrates, the hedgehog gene codes for the fingers and toes on the limbs. It also functions in organizing the brain and the spinal cord. Consequently, mutated hedgehog genes often cause birth defects. Also, if it is activated later in life, certain cancers can be triggered and begin to spread. [5]
In 2006, Beachy moved from Johns Hopkins to Stanford University's Department of Developmental Biology and its Institute for Stem Cell Biology and Regenerative Medicine. He is interested in the function of Hedgehog proteins and other extracellular signals in morphogenesis (pattern formation) and in injury repair and regeneration (pattern maintenance), in particular the normal roles of such signals in stem cell physiology and their abnormal roles in the formation and expansion of cancer stem cells. He is also interested in how the distribution of such signals is regulated in tissues, how cells perceive and respond to distinct concentrations of signals, and how such signaling pathways arose in evolution. [5]
Beachy's research focuses on understanding the molecular mechanisms behind the growth of multicellular embryos, especially the role of the Hedgehog signaling pathway. [7] [8] [9]
Beachy has received numerous awards and prizes for his work, including the Outstanding Young Scientist Award from the Maryland Academy of Sciences in 1997 and the National Academy of Sciences Award in Molecular Biology in 1998. In 2008, Beachy received the March of Dimes Prize in Developmental Biology jointly with Cliff Tabin. [10] In 2011, Beachy received the Keio Medical Science Prize.
Beachy was elected a member of the United States National Academy of Sciences in 2002, and a Fellow of the American Academy of Arts and Sciences (2003). [11]
Beachy is the brother of the historian, Robert M. Beachy, and a cousin of biologist Roger N. Beachy and author Stephen Beachy.
p53, also known as Tumor protein P53, cellular tumor antigen p53, or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins are crucial in vertebrates, where they prevent cancer formation. As such, p53 has been described as "the guardian of the genome" because of its role in conserving stability by preventing genome mutation. Hence TP53 is classified as a tumor suppressor gene.
Cellular differentiation is the process in which a stem cell changes from one type to a differentiated one. Usually, the cell changes to a more specialized type. Differentiation happens multiple times during the development of a multicellular organism as it changes from a simple zygote to a complex system of tissues and cell types. Differentiation continues in adulthood as adult stem cells divide and create fully differentiated daughter cells during tissue repair and during normal cell turnover. Some differentiation occurs in response to antigen exposure. Differentiation dramatically changes a cell's size, shape, membrane potential, metabolic activity, and responsiveness to signals. These changes are largely due to highly controlled modifications in gene expression and are the study of epigenetics. With a few exceptions, cellular differentiation almost never involves a change in the DNA sequence itself. Metabolic composition, however, gets dramatically altered where stem cells are characterized by abundant metabolites with highly unsaturated structures whose levels decrease upon differentiation. Thus, different cells can have very different physical characteristics despite having the same genome.
Sonic hedgehog protein (SHH) is encoded for by the SHH gene. The protein is named after the video game character Sonic the Hedgehog.
In cellular biology, paracrine signaling is a form of cell signaling, a type of cellular communication in which a cell produces a signal to induce changes in nearby cells, altering the behaviour of those cells. Signaling molecules known as paracrine factors diffuse over a relatively short distance, as opposed to cell signaling by endocrine factors, hormones which travel considerably longer distances via the circulatory system; juxtacrine interactions; and autocrine signaling. Cells that produce paracrine factors secrete them into the immediate extracellular environment. Factors then travel to nearby cells in which the gradient of factor received determines the outcome. However, the exact distance that paracrine factors can travel is not certain.
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Zinc finger protein GLI3 is a protein that in humans is encoded by the GLI3 gene.
The Hedgehog signaling pathway is a signaling pathway that transmits information to embryonic cells required for proper cell differentiation. Different parts of the embryo have different concentrations of hedgehog signaling proteins. The pathway also has roles in the adult. Diseases associated with the malfunction of this pathway include cancer.
Smoothened is a protein that in humans is encoded by the SMO gene. Smoothened is a Class Frizzled G protein-coupled receptor that is a component of the hedgehog signaling pathway and is conserved from flies to humans. It is the molecular target of the natural teratogen cyclopamine. It also is the target of vismodegib, the first hedgehog pathway inhibitor to be approved by the U.S. Food and Drug Administration (FDA).
Limb development in vertebrates is an area of active research in both developmental and evolutionary biology, with much of the latter work focused on the transition from fin to limb.
Forkhead box O3, also known as FOXO3 or FOXO3a, is a human protein encoded by the FOXO3 gene.
Indian hedgehog homolog (Drosophila), also known as IHH, is a protein which in humans is encoded by the IHH gene. This cell signaling protein is in the hedgehog signaling pathway. The several mammalian variants of the Drosophila hedgehog gene have been named after the various species of hedgehog; the Indian hedgehog is honored by this one. The gene is not specific to Indian hedgehogs.
Cytonemes are thin, cellular projections that are specialized for exchange of signaling proteins between cells. Cytonemes emanate from cells that make signaling proteins, extending directly to cells that receive signaling proteins. Cytonemes also extend directly from cells that receive signaling proteins to cells that make them.
Matthew P. Scott is an American biologist who was the tenth president of the Carnegie Institution for Science. While at Stanford University, Scott studied how embryonic and later development is governed by proteins that control gene activity and cell signaling processes. He co- discovered homeobox genes in Drosophila melanogaster working with Amy J. Weiner at Indiana University.
Michael B. Elowitz is a biologist and professor of Biology, Bioengineering, and Applied Physics at the California Institute of Technology, and investigator at the Howard Hughes Medical Institute. In 2007 he was the recipient of the Genius grant, better known as the MacArthur Fellows Program for the design of a synthetic gene regulatory network, the Repressilator, which helped initiate the field of synthetic biology. He was the first to show how inherently random effects, or 'noise', in gene expression could be detected and quantified in living cells, leading to a growing recognition of the many roles that noise plays in living cells. His work in Synthetic Biology and Noise represent two foundations of the field of Systems Biology. Since then, his laboratory has contributed to the development of synthetic biological circuits that perform a range of functions inside cells, and revealed biological circuit design principles underlying epigenetic memory, cell fate control, cell-cell communication, and multicellular behaviors.
Philip William Ingham is a British geneticist, currently the Toh Kian Chui Distinguished Professor at the Lee Kong Chian School of Medicine, a partnership between Nanyang Technological University, Singapore and Imperial College, London. Previously, he was the inaugural Director of the Living Systems Institute at the University of Exeter, UK and prior to that was Vice Dean, Research at the Lee Kong Chian School of Medicine.
Clifford James Tabin is chairman of the Department of Genetics at Harvard Medical School.
The evo-devo gene toolkit is the small subset of genes in an organism's genome whose products control the organism's embryonic development. Toolkit genes are central to the synthesis of molecular genetics, palaeontology, evolution and developmental biology in the science of evolutionary developmental biology (evo-devo). Many of them are ancient and highly conserved among animal phyla.
Thomas A. Rando is an American stem cell biologist and neurologist, best known for his research on basic mechanisms of stem cell biology and the biology of aging. He is the Director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research and a professor of Neurology and Molecular, Cell and Developmental Biology at the University of California, Los Angeles. Prior to joining the UCLA faculty, he served as Professor of Neurology and Neurological Sciences at Stanford University School of Medicine, where he was also founding director of the Glenn Center for the Biology of Aging. His additional roles while at Stanford included co-founder and deputy director of the Stanford Center on Longevity, founding director of Stanford's Muscular Dystrophy Association Clinic, and Chief of Neurology at the VA Palo Alto Health Care System.
Kevin Struhl is an American molecular biologist and the David Wesley Gaiser Professor of Biological Chemistry and Molecular Pharmacology at Harvard Medical School. Struhl is primarily known for his work on transcriptional and post transcriptional regulatory mechanisms in yeast using molecular, genetic, biochemical, and genomic approaches. In addition, he has used related approaches to study transcriptional regulatory circuits involved in cellular transformation and the formation of cancer stem cells.