11528 Results for: "2,4-decades-1-ol"

Supplier: Eppendorf

The Innova 40/40R is an easy-to-program orbital shaker that comes with the famous Innova triple eccentric drive to provide 24/7 reliable operation for decades.

Supplier: VWR International

The 4 decade resistance box is a handy and convenient way to investigate resistance.

Supplier: VWR International

This balance is the first major advancement in teaching simple machines in decades.

Supplier: VWR International

Investigating Inductance has never been this easy

Supplier: VWR International

This box changes resistances in a laboratory circuit.

Supplier: Wards

Multiple value resistances with 4mm sockets

Supplier: Wards

Standard decade resistance box.

Supplier: Trajan Scientific and Medical

More than five decades of innovative phase technologies and unique fused silica production capabilities, together provide end-to-end separation solutions for all applications.

Supplier: Bioss

Probably plays an important role in metabolic homeostasis in mitochondria. May function as a nuclear-cytoplasmic shuttling protein that binds transcription factor RELA/NFKB3 in the nucleus and exports it to the cytoplasm. Suppresses p53-induced apoptosis by preventing nuclear localization of RELA.Involvement in disease:Defects in ETHE1 are a cause of ethylmalonic encephalopathy (EE) . EE is an autosomal recessive disorder characterized by neurodevelopmental delay and regression, recurrent petechiae, acrocyanosis, diarrhea, leading to death in the first decade of life. It is also associated with persistent lactic acidemia and ethylmalonic and methylsuccinic aciduria.

Supplier: Trajan Scientific and Medical

More than five decades of innovative phase technologies and unique fused silica production capabilities, together provide end-to-end separation solutions for all applications.

Supplier: Trajan Scientific and Medical

More than five decades of innovative phase technologies and unique fused silica production capabilities, together provide end-to-end separation solutions for all applications.

Supplier: Bioss

Probably plays an important role in metabolic homeostasis in mitochondria. May function as a nuclear-cytoplasmic shuttling protein that binds transcription factor RELA/NFKB3 in the nucleus and exports it to the cytoplasm. Suppresses p53-induced apoptosis by preventing nuclear localization of RELA.Involvement in disease:Defects in ETHE1 are a cause of ethylmalonic encephalopathy (EE) . EE is an autosomal recessive disorder characterized by neurodevelopmental delay and regression, recurrent petechiae, acrocyanosis, diarrhea, leading to death in the first decade of life. It is also associated with persistent lactic acidemia and ethylmalonic and methylsuccinic aciduria.

Supplier: Bioss

Probably plays an important role in metabolic homeostasis in mitochondria. May function as a nuclear-cytoplasmic shuttling protein that binds transcription factor RELA/NFKB3 in the nucleus and exports it to the cytoplasm. Suppresses p53-induced apoptosis by preventing nuclear localization of RELA.Involvement in disease:Defects in ETHE1 are a cause of ethylmalonic encephalopathy (EE) . EE is an autosomal recessive disorder characterized by neurodevelopmental delay and regression, recurrent petechiae, acrocyanosis, diarrhea, leading to death in the first decade of life. It is also associated with persistent lactic acidemia and ethylmalonic and methylsuccinic aciduria.

Supplier: Bioss

Probably plays an important role in metabolic homeostasis in mitochondria. May function as a nuclear-cytoplasmic shuttling protein that binds transcription factor RELA/NFKB3 in the nucleus and exports it to the cytoplasm. Suppresses p53-induced apoptosis by preventing nuclear localization of RELA.Involvement in disease:Defects in ETHE1 are a cause of ethylmalonic encephalopathy (EE) . EE is an autosomal recessive disorder characterized by neurodevelopmental delay and regression, recurrent petechiae, acrocyanosis, diarrhea, leading to death in the first decade of life. It is also associated with persistent lactic acidemia and ethylmalonic and methylsuccinic aciduria.

Supplier: Wards

Ideal for simulating various electrical values.

Supplier: Bioss

Probably plays an important role in metabolic homeostasis in mitochondria. May function as a nuclear-cytoplasmic shuttling protein that binds transcription factor RELA/NFKB3 in the nucleus and exports it to the cytoplasm. Suppresses p53-induced apoptosis by preventing nuclear localization of RELA.Involvement in disease:Defects in ETHE1 are a cause of ethylmalonic encephalopathy (EE) . EE is an autosomal recessive disorder characterized by neurodevelopmental delay and regression, recurrent petechiae, acrocyanosis, diarrhea, leading to death in the first decade of life. It is also associated with persistent lactic acidemia and ethylmalonic and methylsuccinic aciduria.

Supplier: Genetex

Water is a critical component of all living cells. Interestingly, tissue membranes show a great degree of water permeability. Mammalian red cells, renal proximal tubules, and descending thin limb of Henle are extraordinarily permeable to water. Water crosses hydrophobic plasma membranes either by simple diffusion or through a facilitative transport mechanism mediated by special protein ""aquaporin"". Over the last decade, genes for several members of aquaporin family have been cloned, expressed, and their distribution studied in many tissues. AQP0 or MIP26 (major intrinsic protein 26kD), and Aquaporin-1 (AQP1, purified from red cells) also called CHIP-28 (channel forming integral protein, 28kD; 268aa; gene locus 7p14) has been the foundation of the growing family of aquaporin. The lens specific AQP0 represents up to 80% of total lens membrane protein. Defects in MIP26 are cause of autosomal dominant cataract. The cataract Fraser mutation (CAT-FR or Shriveled) is a transposon-induced splicing error that substitutes a long terminal repeat sequence for the c-terminus of MIP. The lens opacity mutation (LOP) is an amino acid substitution that inhibits targeting of MIP to the cell membrane.

Supplier: Thermo Scientific Chemicals

trans,trans-2,4-Decadien-1-ol 90% remainder mainly trans, cis isomer

Supplier: Trajan Scientific and Medical

More than five decades of innovative phase technologies and unique fused silica production capabilities together provide end-to-end separation solutions for all applications.

Supplier: TCI America

CAS Number: 14507-02-9
MDL Number: MFCD00014052
Molecular Formula: C10H18O
Molecular Weight: 154.25
Purity/Analysis Method: >95.0% (GC)
Form: Clear Liquid
Flash Point (°C): 110
Specific Gravity (20/20): 0.87

Supplier: Bioss

Water is a critical component of all living cells. Interestingly, tissue membranes show a great degree of water permeability. Mammalian red cells, renal proximal tubules, and descending thin limb of Henle are extraordinarily permeable to water. Water crosses hydrophobic plasma membranes either by simple diffusion or through a facilitative transport mechanism mediated by special protein "aquaporin". Over the last decade, genes for several members of aquaporin family have been cloned, expressed, and their distribution studied in many tissues. AQP0 or MIP26 (major intrinsic protein 26kD), and Aquaporin 1 (AQP1, purified from red cells) also called CHIP28 (channel forming integral protein, 28kD; 268aa; gene locus 7p14) has been the foundation of the growing family of aquaporin. The lens specific AQP0 represents up to 80% of total lens membrane protein. Defects in MIP26 are cause of autosomal dominant cataract. The cataract Fraser mutation (CATFR or Shriveled) is a transposon induced splicing error that substitutes a long terminal repeat sequence for the C terminus of MIP. The lens opacity mutation (LOP) is an amino acid substitution that inhibits targeting of MIP to the cell membrane.

Supplier: Bioss

Water is a critical component of all living cells. Interestingly, tissue membranes show a great degree of water permeability. Mammalian red cells, renal proximal tubules, and descending thin limb of Henle are extraordinarily permeable to water. Water crosses hydrophobic plasma membranes either by simple diffusion or through a facilitative transport mechanism mediated by special protein "aquaporin". Over the last decade, genes for several members of aquaporin family have been cloned, expressed, and their distribution studied in many tissues. AQP0 or MIP26 (major intrinsic protein 26kD), and Aquaporin 1 (AQP1, purified from red cells) also called CHIP28 (channel forming integral protein, 28kD; 268aa; gene locus 7p14) has been the foundation of the growing family of aquaporin. The lens specific AQP0 represents up to 80% of total lens membrane protein. Defects in MIP26 are cause of autosomal dominant cataract. The cataract Fraser mutation (CATFR or Shriveled) is a transposon induced splicing error that substitutes a long terminal repeat sequence for the C terminus of MIP. The lens opacity mutation (LOP) is an amino acid substitution that inhibits targeting of MIP to the cell membrane.

Supplier: Bioss

Water is a critical component of all living cells. Interestingly, tissue membranes show a great degree of water permeability. Mammalian red cells, renal proximal tubules, and descending thin limb of Henle are extraordinarily permeable to water. Water crosses hydrophobic plasma membranes either by simple diffusion or through a facilitative transport mechanism mediated by special protein "aquaporin". Over the last decade, genes for several members of aquaporin family have been cloned, expressed, and their distribution studied in many tissues. AQP0 or MIP26 (major intrinsic protein 26kD), and Aquaporin 1 (AQP1, purified from red cells) also called CHIP28 (channel forming integral protein, 28kD; 268aa; gene locus 7p14) has been the foundation of the growing family of aquaporin. The lens specific AQP0 represents up to 80% of total lens membrane protein. Defects in MIP26 are cause of autosomal dominant cataract. The cataract Fraser mutation (CATFR or Shriveled) is a transposon induced splicing error that substitutes a long terminal repeat sequence for the C terminus of MIP. The lens opacity mutation (LOP) is an amino acid substitution that inhibits targeting of MIP to the cell membrane.

Supplier: Trajan Scientific and Medical

More than five decades of innovative phase technologies and unique fused silica production capabilities, together provide end-to-end separation solutions for all applications.

Supplier: Prosci

KCTD15 Antibody: Childhood and adult obesity in the United States and to a lesser extent the rest of the world has increased dramatically over the past decade. Both environmental and genetic factors are involved in the onset and progression of weight gain. Recently, the potassium channel KCTD15 was identified as a genetic loci associated with higher than normal body mass index (BMI) in humans along with genes such as GNPDA2, MTCH2, FTO, and TMEM18. Further studies on single nucleotide polymorphisms (SNPs) in non-diabetic and diabetic patients showed that FTO was most strongly associated with obesity while MTCH2 and GNPDA2 were still significantly associated with higher than normal BMI levels. At least two isoforms of KCTD15 are known to exist.

Supplier: Prosci

KCTD15 Antibody: Childhood and adult obesity in the United States and to a lesser extent the rest of the world has increased dramatically over the past decade. Both environmental and genetic factors are involved in the onset and progression of weight gain. Recently, the potassium channel KCTD15 was identified as a genetic loci associated with higher than normal body mass index (BMI) in humans along with genes such as GNPDA2, MTCH2, FTO, and TMEM18. Further studies on single nucleotide polymorphisms (SNPs) in non-diabetic and diabetic patients showed that FTO was most strongly associated with obesity while MTCH2 and GNPDA2 were still significantly associated with higher than normal BMI levels. At least two isoforms of KCTD15 are known to exist.

Supplier: TCI America

CAS Number: 59376-58-8
MDL Number: MFCD00014053
Molecular Formula: C11H20O
Molecular Weight: 168.28
Purity/Analysis Method: >95.0% (GC)
Form: Clear Liquid
Color: Very Pale Yellow
Flash Point (°C): 110
Specific Gravity (20/20): 0.88

Supplier: Bioss

Defects in PANK2 are the cause of neurodegeneration with brain iron accumulation type 1 (NBIA1); also known as pantothenate kinase-associated neurodegeneration (PKAN) or Hallervorden-Spatz syndrome (HSS). It is an autosomal recessive neurodegenerative disorder associated with iron accumulation in the brain, primarily in the basal ganglia. Clinical manifestations include progressive muscle spasticity, hyperreflexia, muscle rigidity, dystonia, dysarthria, and intellectual deterioration which progresses to severe dementia over several years. It is clinically classified into classic, atypical, and intermediate phenotypes. Classic forms present with onset in the first decade, rapid progression, loss of independent ambulation within 15 years. Atypical forms have onset in the second decade, slow progression, maintenance of independent ambulation up to 40 years later. Intermediate forms manifest onset in the first decade with slow progression or onset in the second decade with rapid progression. Patients with early onset tend to also develop pigmentary retinopathy, whereas those with later onset tend to also have speech disorders and psychiatric features. All patients have the 'eye of the tiger' sign on brain MRI.Defects in PANK2 are the cause of hypoprebetalipoproteinemia, acanthocytosis, retinitis pigmentosa, and pallidal degeneration (HARP). HARP is a rare syndrome with many clinical similarities to NBIA1.

Supplier: Bioss

Defects in PANK2 are the cause of neurodegeneration with brain iron accumulation type 1 (NBIA1); also known as pantothenate kinase-associated neurodegeneration (PKAN) or Hallervorden-Spatz syndrome (HSS). It is an autosomal recessive neurodegenerative disorder associated with iron accumulation in the brain, primarily in the basal ganglia. Clinical manifestations include progressive muscle spasticity, hyperreflexia, muscle rigidity, dystonia, dysarthria, and intellectual deterioration which progresses to severe dementia over several years. It is clinically classified into classic, atypical, and intermediate phenotypes. Classic forms present with onset in the first decade, rapid progression, loss of independent ambulation within 15 years. Atypical forms have onset in the second decade, slow progression, maintenance of independent ambulation up to 40 years later. Intermediate forms manifest onset in the first decade with slow progression or onset in the second decade with rapid progression. Patients with early onset tend to also develop pigmentary retinopathy, whereas those with later onset tend to also have speech disorders and psychiatric features. All patients have the 'eye of the tiger' sign on brain MRI.Defects in PANK2 are the cause of hypoprebetalipoproteinemia, acanthocytosis, retinitis pigmentosa, and pallidal degeneration (HARP). HARP is a rare syndrome with many clinical similarities to NBIA1.

Supplier: Genetex

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is well known as one of the key enzymes involved in glycolysis. Besides its functioning as a glycolytic enzyme in cytoplasm, recent evidence suggest that mammalian GAPDH is also involved in a great number of intracellular processes such as membrane fusion, microtubule bundling, phosphotransferase activity, nuclear RNA export, DNA replication, and DNA repair. During the last decade a lot of findings appeared concerning the role of GAPDH in different pathologies including prostate cancer progression, programmed neuronal cell death, age-related neuronal diseases, such as Alzheimer's and Huntington's disease. GAPDH is constitutively expressed in almost all tissues at high levels, therefore becoming the marker of choice when a loading control in Western blotting is required. Some physiological factors, such as hypoxia and diabetes, increase GAPDH expression in certain cell types.