Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Explain how the binding of a ligand initiates signal transduction throughout a cellRecognize the role of phosphorylation in the transmission of intracellular signalsEvaluate the role of second messengers in signal transmission

Life as an emergent property of networks of chemical reactions involving proteins and nucleic acids. Mathematical theories of metabolism, gene regulation, signal transduction, chemotaxis, excitability, motility, mitosis, development, and immunity. Applications to directed molecular evolution, DNA computing, and metabolic and genetic engineering.

This course covers cells and tissues of the immune system, lymphocyte development, the structure and function of antigen receptors, the cell biology of antigen processing and presentation, including molecular structure and assembly of MHC molecules, the biology of cytokines, leukocyte-endothelial interactions, and the pathogenesis of immunologically mediated diseases. The course is structured as a series of lectures and tutorials in which clinical cases are discussed with faculty tutors.
Lecturers
Frederick W. Alt, Marcus Altfeld, Paul Anderson, Jon C. Aster, Hugh Auchincloss, Steven P. Balk, Samuel M. Behar, Richard S. Blumberg, Francisco Bonilla, Bobby Cherayil, Benjamin Davis, David Hafler, Nir Harcohen, Bruce Horwitz, David M. Lee, Andrew Lichtman, Diane Mathis, Richard Mitchell, Hidde Ploegh, Emmett Schmidt, Arlene Sharpe, Megan Sykes, Shannon Turley, Dale T. Umetsu, Ulrich von Andrian, Bruce Walker, Kai Wucherpfennig, Ramnik Xavier, Sarah Henrickson

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"In endocytosis, the cell plasma membrane folds inward and pinches off to form intracellular vesicles. Originally, endocytosis was thought to primarily facilitate feeding and pathogen neutralization, but it is now known to regulate numerous processes in eukaryotic cells, such as signaling, membrane composition, mitosis, movement, and morphogenesis. Endocytosis also plays many roles in T cells through both clathrin-dependent and clathrin-independent mechanisms. For example, clathrin-mediated endocytosis regulates the receptors on the plasma membrane and internalizes α/β-type T cell antigen receptors (TCRs). Through clathrin-independent pathways, endocytosis internalizes TCRζ and the IL-2Rβ complex and recycles TCRαβ. Clathrin-independent endocytosis also helps T cells bind to antigen-presenting cells of the immune system and ingest pathogens and other foreign materials to aid in host defense and immune surveillance..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This seminar-format course provides an in-depth presentation and discussion of how engineering and biological approaches can be combined to solve problems in science and technology, emphasizing integration of biological information and methodologies with engineering analysis, synthesis, and design. Emphasis is placed on molecular mechanisms underlying cellular processes, including signal transduction, gene expression networks, and functional responses.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"G protein-coupled receptors (GPCRs) are key proteins that help transmit extracellular signals into cells. Arrestin molecules help regulate GPCR signaling by recognizing and binding to GPCR residues that have been phosphorylated specifically by the kinase GRK. Two models, the barcode model and the flute model, have been proposed to explain this process. In the barcode model, different protein kinases produce different phosphorylation “barcodes” on GPCRs and arrestins “read” the barcodes produced by GRK to produce certain signaling outcomes. In the flute model, different phosphorylation patterns form different sequences of “notes”. These notes can then be “played” in various ways by the different structural features of arrestins, enabling multiple “songs” (outcomes) to be produced from one set of notes..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The transcription factor CREB plays an important role in the development of pulmonary hypertension (PH). However, both increased and decreased CREB expression have been proposed to mediate the proliferation of pulmonary artery smooth muscle cells (PASMCs). Additionally, the regulatory signaling of CREB activation in PASMCs proliferation has not been well characterized in PH. Researchers recently used various in vitro techniques to clarify CREB’s role. CRE-containing genes were upregulated in PH PASMCs, and total and phosphorylated CREB protein levels were elevated in PASMCs from rats with monocrotaline (MCT)-induced PH. Prolonged upregulation of serum-induced CREB phosphorylation was also observed in hypoxia-pretreated PASMCs. These results may have been due to activation of multiple protein kinases and downregulation of numerous phosphatases targeting CREB..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Dysregulation of the IL-6-induced JAK/STAT cascade is associated with severe inflammatory and proliferative diseases. The cascade is normally tightly controlled by proteins such as the feedback inhibitor SOCS3 and the tyrosine phosphatase SHP2. SOCS3 increases the stability of late IL-6-induced STAT3 activation across cells with different STAT3 levels and reduces the signal magnitude. but whether SHP2 similarly affects robustness and information transfer remains unclear. Researchers recently used multiplexed single-cell analyses and information theory approaches to clarify SHP2’s roles. They found that SHP2 improved the robustness of STAT3 activation under basal conditions (in the absence of the cytokine IL-6) and during early IL-6 signalling levelling the degree of activation across cells with heterogeneous expression levels of STAT3. However, it did not affect the robustness of late IL-6-induced STAT3 activation..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This is a seminar based on research literature. Papers covered are selected to illustrate important problems and approaches in the field of computational and systems biology, and provide students a framework from which to evaluate new developments.
The MIT Initiative in Computational and Systems Biology (CSBi) is a campus-wide research and education program that links biology, engineering, and computer science in a multidisciplinary approach to the systematic analysis and modeling of complex biological phenomena. This course is one of a series of core subjects offered through the CSB Ph.D. program, for students with an interest in interdisciplinary training and research in the area of computational and systems biology.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The tyrosine kinase p56 Lck is critical for T-cell development and activation. Lck initiates signaling events downstream of the T-cell receptor (TCR) by phosphorylating ITAM motifs located within CD3 chains, which in turn recruits the kinase Zap-70 to the activated TCR/CD3 complex. But while the regulation of its enzymatic activity is mostly attributed to two tyrosine residues, Y394 and Y505, Lck has an additional highly conserved tyrosine, Y192, whose function in the regulation of Lck activity is not fully understood. A recent study examined the role of this residue in primary T cells and T cell lines. Using knock-in mice expressing a phosphomimetic mutant of Lck (LckY192E), researchers found that Lck Y192E bound poorly to CD45 and showed hyperphosphorylation at Y505, similar to previous data in Jurkat cell lines. However, in vitro, Lck Y192E had normal enzymatic activity in both human and mouse T cells, suggesting that this residue acts independently of the interaction with CD45..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Undernourishment or undernutrition can be caused by a lack of food or a high energy demand, such as during pregnancy and lactation. Undernutrition in production animals disrupts metabolic homeostasis and causes serious health problems, including maternal metabolic disorders and stillbirth. Many production animals are ruminants, named for their unique digestive organ, the rumen, which houses a diverse anaerobic microbiome. The ruminal microbiome allows the host to break down hard-to-digest plant carbohydrates and produce protein that the host later absorbs. But little is known about the effects of undernutrition on the host-microbiome interaction in ruminants. A recent study investigated changes in the ruminal microbiome and epithelium in undernourished pregnant sheep. During undernutrition, the bacterial genes involved in the digestion of carbohydrates and protein synthesis were downregulated. This meant less energy and protein was available to the host and critical signaling pathways were inhibited..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Peptide hormones are important signaling molecules within the body. One such peptide is the secreted protein augurin, which is encoded by the gene Ecrg4, whose expression has been reported in a wide range of human tissues. The product of the gene Ecrg4, the augurin precursor ECRG4, has been predicted to be cleaved to originate different peptides. Augurin is implicated in a variety of processes, including tumorigenesis, inflammation, and infection. It is also involved in the regulation of the hypothalamo-pituitary adrenal axis and in osteoblast differentiation. Augurin is implicated in the modulation of well-known signaling cascades, including NF-kB, PI3K/Akt/mTor, Wnt-beta catenin, and apoptosis pathways, however, the molecular mechanisms underlying its action remain largely unexplored. Given its involvement in health and disease, augurin is an attractive target for the discovery of new therapeutic agents for human pathologies..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.