Inhibition Definition Biology

C O N T E N T S:

KEY TOPICS

  • While further work will be required to explore the applications of these proteins in cellular systems, one attractive area in ssDNA biology is to manipulate telomerase and telomeres in general.(More…)
  • Berridge M, Herst P, Tan A. Tetrazolium dyes as tools in cell biology: new insights into their cellular reduction.(More…)
  • Taken at its simplest definition, the term “necrosis” simply refers to a mass of dead cells, and is independent of the cell death pathway followed to reach that point.(More…)

POSSIBLY USEFUL

  • This inhibition of an enzyme by a product of its pathway is a form of negative feedback.(More…)

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Inhibition Definition Biology
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KEY TOPICS

While further work will be required to explore the applications of these proteins in cellular systems, one attractive area in ssDNA biology is to manipulate telomerase and telomeres in general. [1] In this study we have shown that we have the ability to design proteins that recognise specific ssDNA sequences of interest, with many potential applications in biology and biotechnology. [1]

Wright AV, Nunez JK, Doudna JA. Biology and applications of CRISPR systems: harnessing nature’s toolbox for genome engineering. [1]

“Complement biology,” In Hoffman R, Benz EJ, Shattil SJ, Furie B, Cohen HJ, Silberstein LE, McGlave P, (eds.) (2000). [2]

The addition of a telomeric sequence-specific cPPR in cells could be useful to skew this competition by blocking telomerase access and preventing telomere extension—to study telomere biology and as potential cancer therapeutics in the future. [1] This opens up new opportunities to engineer artificial telomere-protective proteins and to understand fundamental aspects of telomere biology. [1] If combined with protein signals to efficiently target cPPRs to regions of the cell containing their ssDNA targets, these proteins could help reveal the many aspects of cell biology involving ssDNA, which are currently understudied due to a lack of appropriate tools. [1]

Berridge M, Herst P, Tan A. Tetrazolium dyes as tools in cell biology: new insights into their cellular reduction. [3] NKT cell-TCR expression activates conventional T cells in vivo, but is largely dispensable for mature NKT cell biology. [3]

This powerful ability to induce gene transcription has made IPTG a technology that has revolutionized biology across many fields, including the study and treatment of diseases. [4] The creation of disease models for the study of the pathology observed in complex and devastating human illnesses, including leishmaniasis, is necessary and is becoming achievable with the emergence of synthetic biology and IPTG induction. [4] The re-design and application of IPTG induction of gene expression in synthetic biology is certainly promising for our pursuit of understanding biological mechanisms and disease. [4] Synthetic biology is changing how we study disease by redesigning a powerful biological system, the inducible gene expression system. [4] Fortunately, dangerous diseases, such as leishmaniasis, are being combated by a new emerging field called synthetic biology that is defined as “the design and construction of new biological parts, devices, and systems, or the re-design of existing, natural biological systems for useful purposes,” and requires the merging of biology, mathematics and engineering. [4]

Today, one of the most important inducible gene expression systems being used in synthetic biology is the induction of the lac operon by the compound isopropyl ?-D-1-thiolgalactopyranoside (IPTG). [4]

Mackessy, S.P. (2002) Toxinology of colubrid snakes: biology, venoms and envenomation. [5] Biology of the sea snakes and biochemistry of their venoms. [5]

Taken at its simplest definition, the term “necrosis” simply refers to a mass of dead cells, and is independent of the cell death pathway followed to reach that point. [3] This process of manufacturing protein products from DNA is the very definition of a gene expression system. [4] In a narrow definition, virucidal activity represents the activity by which to interact with and physically disrupt viral particles. [6] In a broad definition, it includes the activity by which to functionally inhibit (neutralize) viral infectivity without apparent morphological alterations of the viral particles. [6] In this article, we describe methods to assess virucidal activity in a broad definition. [6]

POSSIBLY USEFUL

This inhibition of an enzyme by a product of its pathway is a form of negative feedback. [7] Allosteric control can involve stimulation of enzyme action as well as inhibition. [7] Allosteric stimulation and inhibition allow production of energy and materials by the cell when they are needed and inhibit production when the supply is adequate. [7]

Protein concentrations used were, from left to right: 0, 0.15, 0.3, 0.5, 1, 2, 4, 6, 8 and 10 µM. c Inhibition of telomerase extension by telomere-targeting cPPRs in telomerase activity assays with immunopurified telomerase and a primer incorporating 18 nt of telomeric sequence. [1] Inhibition of telomerase extension was maintained even when non-specific competitor ssDNA was present in orders of magnitude excess (Supplementary Fig.   6 ). [1] The potent inhibition of telomerase likely results from the cPPR’s ability to block access of telomerase to ssDNA, since we found that cPPR-Telo2 could protect its ssDNA target from DNase I digestion (Supplementary Fig.   7b ). [1] Competitive inhibition occurs when molecules very similar to the substrate molecules bind to the active site and prevent binding of the actual substrate. [7] In some cases of noncompetitive inhibition, the inhibitor is thought to bind to the enzyme in such a way as to physically block the normal active site. [7] Noncompetitive inhibition occurs when an inhibitor binds to the enzyme at a location other than the active site. [7] This latter type of noncompetitive inhibition is called allosteric inhibition ; the place where the inhibitor binds to the enzyme is called the allosteric site. [7] Feedback inhibition is usually accomplished through something called an “allosteric site” a site on an enzyme that changes the shape of an enzyme, and subsequently the behavior of the active site. [8] In feedback inhibition, binding of the end product to the allosteric site slows down or stops the enzyme’s activity so that little or no new end product is produced. [8] Feedback inhibition prevents waste that occurs when more of a product is made than the cell needs. It can also prevent harm when having too much of the pathway’s end product may actually be harmful to the organism. [8] The result of feedback inhibition is This allows them to adjust their rate of reaction depending on how much of their end product is needed, and prevent their end product from building up to dangerous levels. [8] In feedback inhibition, a biochemical pathway is inhibited by its own end product. [8] In some people, dangerously high cholesterol can be a result of this feedback inhibition pathway getting turned off – resulting in the body continuing to produce its own cholesterol in addition to what is consumed. [8] Typically, feedback inhibition acts on the first enzyme unique to a given pathway. [8] The enzymes that produce ATP from glucose are subject to feedback inhibition by ATP. This saves glucose by preventing its unnecessary breakdown when the cell has plenty of ATP. [8]

Without feedback inhibition, energy or raw materials that could be used for important cellular functions might be wasted on unnecessary ones. [8] Without feedback inhibition, raw materials and energy might be depleted by biochemical processes that don’t stop, even when their end product is not needed. [8]

Some cases of dangerously high cholesterol are caused by failure of this feedback inhibition mechanism, resulting in large amounts of cholesterol being made by the liver even though there is already a large amount of cholesterol present in the body. [8]

Their action can be overcome by increasing the substrate concentration and at high enough substrate concentrations competitive inhibition cannot be observed and the rate of reaction is essentially Vmax. [9]

Inhibition of proteasome activity promotes the correct localization of disease-causing alpha-sarcoglycan mutants in HEK-293 cells constitutively expressing beta-, gamma-, and delta-sarcoglycan. [3] Chapelsky S, Batty S, Frost M, Mogridge J. Inhibition of anthrax lethal toxin-induced cytolysis of RAW264.7 cells by celastrol. [3] Guo S, Miyake M, Liu K, Shi H. Specific inhibition of hypoxia inducible factor 1 exaggerates cell injury induced by in vitro ischemia through deteriorating cellular redox environment. [3]

IPTG inhibition prevents the use of both systems in the same cell. [4] Inhibition of the TAM family in the tumor microenvironment (TME) activates the immune system in the TME, reverses TAM mediated immunosuppression and enhances the anti-tumor immune response, which lead to immune-mediated tumor cell killing. [10] Inhibition of metastatic outgrowth from single dormant tumor cells by targeting the cytoskeleton. [3]

Inhibition of transcriptase activity of influenza A virus in vitro by anti-haemagglutinin antibodies. [6] A new C-type lectin (RVsnaclec) purified from venom of Daboia russelii russelii shows anticoagulant activity via inhibition of FXa and concentration-dependent differential response to platelets in a Ca 2+ -independent manner. [5]

A typical sigmoid curve showing inhibition of viral infectivity by serial dilutions of an antiviral drug. [6] Determination of 50% inhibitory concentration (IC 50 ): IC 50 of an antiviral substance against a given virus can be obtained based on the percent inhibition of viral infectivity mediated by serial dilutions of the antiviral substance. [6]

This inhibition of the enzyme essentially increases neurotransmission at synapses that release acetylcholine. [11] Inhibition of pyruvate kinase M2 by reactive oxygen species contributes to cellular antioxidant responses. [3] Synergistic inhibition of head and neck tumor growth by green tea (-)-epigallocatechin-3-gallate and EGFR tyrosine kinase inhibitor. [3]

RANKED SELECTED SOURCES(11 source documents arranged by frequency of occurrence in the above report)

1. (11) Feedback Inhibition – Definition, Function and Examples | Biology Dictionary

2. (9) Modular ssDNA binding and inhibition of telomerase activity by designer PPR proteins

3. (9) Cell Based Assays: the Cell Cycle, Cell Proliferation and Cell Death

4. (8) Shared Results – Deadly Diseases, Synthetic Biology, and IPTG – Gold Biotechnology

5. (7) enzyme | Definition, Mechanisms, & Nomenclature | Britannica.com

6. (6) Virucidal and Neutralizing Activity Tests for Antiviral Substances and Antibodies –BIO-PROTOCOL

7. (3) Steve Mackessy, Professor , School of Biological Sciences, Natural and Health Sciences

8. (1) Definition of TAM/c-Met inhibitor RXDX-106 – NCI Drug Dictionary – National Cancer Institute

9. (1) 35.2: How Neurons Communicate – Biology LibreTexts

10. (1) Complement system – Wikipedia

11. (1) Competitive and noncompetitive enzyme inhibitors differ with respect to | Study.com