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Mutations in these photo receptors and their signal transduction components lead to seedling development that is at odds with light conditions, for example seedlings that show photomorphogenesis when grown in the dark.
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Mutations and these
Mutations in these proteins can result in altered functionality of sub-complex assembly, copper transport, or translational regulation.
Mutations periodically occur within the Y chromosome and these mutations are passed on to males in subsequent generations.
Mutations in the autosomal RET proto-oncogene drives these malignancies
Mutations in these areas can lead to non-functional proteins that can polymerise and accumulate in the liver ( infantile hepatic cirrhosis ).
Mutations in these genes account for 70 to 80 percent of all cases of cerebral cavernous malformations.
Mutations in the DNA binding regions for either of these proteins results in ablation of transgene GLUT-4 expression.
Mutations in the surface proteins allow the virus to elude some host immunity, and the numbers and locations of these mutations that confer the greatest amount of immune escape has been an important topic of study for over a decade.
Mutations in the PCCA or PCCB genes disrupt the function of the enzyme, preventing these acids from being metabolized.
COUM's earliest public events were impromptu musical gigs performed at various pubs around Hull ; titles for these events included Thee Fabulous Mutations, Space Between the Violins, Dead Violins and Degradation and Clockwork Hot Spoiled Acid Test.
Mutations in any of these genes prevent the proper production or assembly of the type IV collagen network, which is an important structural component of basement membranes in the kidney, inner ear, and eye.
Mutations of all these proteins are associated with both atrial and ventricular septal defects ; In addition, NKX2-5 is associated with defects in the electrical conduction of the heart and TBX5 is related to the Holt-Oram syndrome which includes electrical conduction defects and abnormalities of the upper limb.
Mutations that affect the normal function of these genes can result in retinitis pigmentosa and vision loss.
Mutations in the genes for these keratins are associated with epidermolysis bullosa simplex and Dermatopathia pigmentosa reticularis, both of which are autosomal dominant mutations.
Mutations in these genes typically lead to the synthesis of a truncated EXT protein which does not function normally.
Mutations in either of these genes disrupt the ability of this transporter protein to reabsorb these amino acids, allowing them to become concentrated in the urine.
Mutations in these cells are transmitted to offspring, while, on the other hand, those in somatic cells are not.
Mutations of the CFTR gene affect functioning of the chloride ion channels in these cell membranes, leading to cystic fibrosis and congenital absence of the vas deferens.
Mutations in these transporter proteins lead to a rare congenital disease called sitosterolaemia, which is characterised by:
Mutations in these genes alter the usual structure and function of potassium channels or prevent the assembly of normal channels.
Mutations in any of these genes alter the structure or function of channels, which changes the flow of ions between cells.
Mutations in any of these genes disrupt the production, processing, or assembly of type II or type XI collagen.
Mutations in any of these genes reduce or eliminate the function of the enzyme complex, preventing the normal breakdown of isoleucine, leucine, and valine.
Mutations cause reductions in these functional proteins but, it is unclear exactly how a shortage in these proteins leads to incomplete separation of the vertebrae in people with Klippel-Feil syndrome.
Mutations and receptors
Mutations in receptors that result in increased constitutive activity underlie some inherited diseases, such as precocious puberty ( due to mutations in luteinizing hormone receptors ) and hyperthyroidism ( due to mutations in thyroid-stimulating hormone receptors ).
Mutations and their
Mutations in viral genes weakened their infectious ability, sometimes creating viruses that were able to infect and grow within only certain varieties of E coli.
Mutations that make organisms more adapted to their environment increase in the population through natural selection as organisms with favorable mutations have more offspring.
*" Mutations ", a song by Salt the Wound from their 2009 album, Ares
Mutations in BMPs and their inhibitors ( such as sclerostin ) are associated with a number of human disorders which affect the skeleton.
# REDIRECT Fallout ( series )# Mutations and their causes
Mutations in proto-oncogenes, which are the normally quiescent counterparts of oncogenes, can modify their expression and function, increasing the amount or activity of the product protein.
Mutations in proto-oncogenes can modify their expression and function, increasing the amount or activity of the product protein.
Mutations and signal
Mutations in position 816 of c-kit can result in a constant division signal being sent to the mast cells, resulting in abnormal proliferation.
Mutations and components
Mutations in the upstream components of the ERK5 pathway ( the CCM complex ) are thought to underlie cerebral cavernous malformations in humans.
Mutations and lead
Mutations in the gene HR can lead to complete hair loss, though this is not typical in humans.
Mutations in such microRNAs ( known as oncomirs ) can lead to activation of oncogenes.
Mutations in transpeptidases that lead to reduced interactions with an antibiotic are a significant source of emerging antibiotic resistance.
Mutations may also lead to fewer copies of the CFTR protein being produced.
Mutations of mitochondrial DNA can lead to a number of illnesses including exercise intolerance and Kearns-Sayre syndrome ( KSS ), which causes a person to lose full function of heart, eye, and muscle movements.
Mutations in different parts of the gene may lead to deafness or Stickler syndrome type III ( eye problems: myopia, retinal detachment and skeletal abnormalities ).
Mutations in the gene may cause impaired transport of lipids in the skin layer and may also lead to small version of the proteins responsible for skin development.
Mutations that reduce the production of functional myostatin lead to an overgrowth of muscle tissue.
Mutations in the gene encoding this protein lead to Meesmann corneal dystrophy.
Mutations in the gene encoding this protein lead to Jackson-Lawler type pachyonychia congenita and steatocystoma multiplex.
Mutations in the dystrophin gene that lead to the production of less defective, but still only partially functional dystrophin protein, result in a display of a much milder dystrophic phenotype in affected patients, resulting in the disease known as Becker's muscular dystrophy ( BMD ).
Mutations in the ceruloplasmin gene (< i > CP </ i >), which are very rare, can lead to the genetic disease aceruloplasminemia, characterized by hyperferritinemia with iron overload.
Mutations in TCOF1 lead to haploinsufficiency of the Treacle protein.
Mutations in the PROS1 gene can lead to Protein S deficiency which is a rare blood disorder which can lead to an increased risk of thrombosis.
Mutations in the HADHA gene lead to inadequate levels of an enzyme called long-chain 3-hydroxyacyl-coenzyme A ( CoA ) dehydrogenase, which is part of a protein complex known as mitochondrial trifunctional protein.
Mutations in the gene can lead to a defective protein and several forms of inherited arrhythmias as Long QT syndrome which is a prolongation of the QT interval of heart repolarization, Short QT syndrome, and Familial Atrial Fibrillation.
Mutations that lead to EGFR overexpression ( known as upregulation ) or overactivity have been associated with a number of cancers, including lung cancer, anal cancers and glioblastoma multiforme.
Mutations involving EGFR could lead to its constant activation, which could result in uncontrolled cell division – a predisposition for cancer.
Mutations in these domains lead to the channel's desensitivity to the βγ-complex and therefore reduce the activation of the GIRK channel.
Mutations in genes encoding these proteins can lead to inactivation of cadherin cell adhesions and elimination of contact inhibition, allowing cells to proliferate and migrate, thus promoting tumorigenesis and cancer development.
Mutations in DNA that lead to cancer ( only certain mutations can lead to cancer and the majority of potential mutations will have no bearing ) disrupt these orderly processes by disrupting the programming regulating the processes.
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