234440 Results for: "Amberlyst® 15 H\u207A form"

Supplier: TECHNICAL QUARTZ SOLUTIONS

Made of silica.

Supplier: Bioss

RuBisCO catalyzes two reactions: the carboxylation of D-ribulose 1,5-bisphosphate, the primary event in carbon dioxide fixation, as well as the oxidative fragmentation of the pentose substrate in the photorespiration process. Both reactions occur simultaneously and in competition at the same active site.Sequence similarities: Belongs to the RuBisCO large chain family. Type I subfamily.Post-translational modifications: The disulfide bond which can form between Cys-247 in the large chain dimeric partners within the hexadecamer appears to be associated with oxidative stress and protein turnover (By similarity). The disulfide bonds reported in 1RBO may be the result of oxidation during crystallization.

Supplier: Bioss

RuBisCO catalyzes two reactions: the carboxylation of D-ribulose 1,5-bisphosphate, the primary event in carbon dioxide fixation, as well as the oxidative fragmentation of the pentose substrate in the photorespiration process. Both reactions occur simultaneously and in competition at the same active site.Sequence similarities: Belongs to the RuBisCO large chain family. Type I subfamily.Post-translational modifications: The disulfide bond which can form between Cys-247 in the large chain dimeric partners within the hexadecamer appears to be associated with oxidative stress and protein turnover (By similarity). The disulfide bonds reported in 1RBO may be the result of oxidation during crystallisation.

Supplier: Bioss

RuBisCO catalyzes two reactions: the carboxylation of D-ribulose 1,5-bisphosphate, the primary event in carbon dioxide fixation, as well as the oxidative fragmentation of the pentose substrate in the photorespiration process. Both reactions occur simultaneously and in competition at the same active site.Sequence similarities: Belongs to the RuBisCO large chain family. Type I subfamily.Post-translational modifications: The disulfide bond which can form between Cys-247 in the large chain dimeric partners within the hexadecamer appears to be associated with oxidative stress and protein turnover (By similarity). The disulfide bonds reported in 1RBO may be the result of oxidation during crystallization.

Supplier: Bioss

RuBisCO catalyzes two reactions: the carboxylation of D-ribulose 1,5-bisphosphate, the primary event in carbon dioxide fixation, as well as the oxidative fragmentation of the pentose substrate in the photorespiration process. Both reactions occur simultaneously and in competition at the same active site.Sequence similarities: Belongs to the RuBisCO large chain family. Type I subfamily.Post-translational modifications: The disulfide bond which can form between Cys-247 in the large chain dimeric partners within the hexadecamer appears to be associated with oxidative stress and protein turnover (By similarity). The disulfide bonds reported in 1RBO may be the result of oxidation during crystallization.

Supplier: Thermo Fisher Scientific

Provides a source of iron used in cell culture applications. Provides iron in a less toxic form than free iron salts.

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: VWR Collection

PTFE, with spout.

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: Cayman Chemical

Calcein is a xanthene that is commonly used for the fluorometric determination of calcium in solution. As this form of calcein is not membrane permeable, it can be used in assays that evaluate membrane integrity. Calcein can also be used as a fluorescent indicator for fluoride, iron, and mercury. Excitation and emission maxima for calcein are 494 and 517 nm, respectively.

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: RSG

Double-ended spoons made from stainless steel.

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: Thermo Fisher Scientific

These crucibles are manufactured from platinum. Available in standard form.

Supplier: Bioss

HEAT repeats form rod-like helical structures that are involved in intracellular transport. HEATR7B2 (HEAT repeat-containing protein 7B2) is a 1,585 amino acid protein that contains fifteen HEAT repeats. Existing as two alternatively spliced isoforms, the gene encoding HEATR7B2 maps to human chromosome 5p13.1 and mouse chromosome 15 A1. Chromosome 5 contains 181 million base pairs and comprises nearly 6% of the human genome. Cockayne syndrome is associated with chromosome 5 through the ERCC8 gene and familial adenomatous polyposis via the adenomatous polyposis coli (APC) tumor suppressor gene. Treacher Collins syndrome is also chromosome 5-associated and is caused by insertions or deletions within the TCOF1 gene. Deletion of the p arm of chromosome 5 leads to Cri du chat syndrome, while deletion of the q arm or of chromosome 5 altogether is common in therapy-related acute myelogenous leukemias and myelodysplastic syndrome.

Supplier: GLASWARENFABRIK KARL HECHT

Made of borosilicate glass.

Supplier: Bioss

Cellular receptors for blood proteases regulate chemotaxis, extracellular proteolysis, and growth behavior of normal and malignant cells. Effector cell protease receptor-1 (EPR1) is a receptor for the coagulation protease factor Xa. EPR1 is characterized by a cysteine-rich extracellular module, a single membrane-spanning domain, and a serine-rich cytoplasmic tail featuring at least 15 potential phosphorylation sites. EPR1 also contains 2 N-linked glycosylation sites, 4 O-linked glycosylation sites, and a chondroitin sulfate attachment site, which may provide anchoring for carbohydrate chains, EPR1 transfectants bind to factor Xa in a specific and saturable manner, and in the absence of factor V/Va promote prothrombin activation in a factor Xa concentration-dependent reaction. Activated platelets and megakaryocytes express EPR1. Both EPR1 and membrane-bound factor Va are thought to be required to mediate factor Xa binding to the activated platelet to form a functional prothrombinase complex.

Supplier: ENZO LIFE SCIENCES

Inhibitor of a variety of serine/threonine and tyrosine kinases, like protein kinase C (PKC), cyclic AMP-dependent protein kinase (PKA), S6 kinase, Akt (protein kinase B; PKB), epidermal growth factor receptor (EGFR) tyrosine kinase activity and others including KDR, VEGFR, PDGFR, c-kit and other receptor tyrosine kinases. Potently inhibits FLT-3 kinase including mutant forms found in acute myeloid leukemia in vitro and in vivo. Apoptosis inducer. Showed broad antiproliferative activity against various tumor cell lines. Selectively inhibits T lymphocyte production of TNF-α. Upregulates endothelial nitric oxide synthase (eNOS; NOS III). Abrogates tumor angiogenesis in vivo.

Supplier: ProSci Inc.

Mucin-15 is a single-pass type I membrane protein member of the Mucin family. Mucins are a family of high molecular weight, heavily glycosylated proteins (glycoconjugates) produced by epithelial tissues in most metazoans. A key characteristic of Mucins is their ability to form gels. Therefore they are a key component in most gel-like secretions, serving functions from lubrication to cell signalling to forming chemical barriers. Mucin-15 is expressed in many tissues. Mucin-15 is highly glycosylated (N- and O-linked carbohydrates). Mucin-15 may play a role in the cell adhesion to the extracellular matrix.

Supplier: Bioss

Cellular receptors for blood proteases regulate chemotaxis, extracellular proteolysis, and growth behavior of normal and malignant cells. Effector cell protease receptor-1 (EPR1) is a receptor for the coagulation protease factor Xa. EPR1 is characterised by a cysteine-rich extracellular module, a single membrane-spanning domain, and a serine-rich cytoplasmic tail featuring at least 15 potential phosphorylation sites. EPR1 also contains 2 N-linked glycosylation sites, 4 O-linked glycosylation sites, and a chondroitin sulfate attachment site, which may provide anchoring for carbohydrate chains, EPR1 transfectants bind to factor Xa in a specific and saturable manner, and in the absence of factor V/Va promote prothrombin activation in a factor Xa concentration-dependent reaction. Activated platelets and megakaryocytes express EPR1. Both EPR1 and membrane-bound factor Va are thought to be required to mediate factor Xa binding to the activated platelet to form a functional prothrombinase complex.

Supplier: Bioss

Cellular receptors for blood proteases regulate chemotaxis, extracellular proteolysis, and growth behavior of normal and malignant cells. Effector cell protease receptor-1 (EPR1) is a receptor for the coagulation protease factor Xa. EPR1 is characterised by a cysteine-rich extracellular module, a single membrane-spanning domain, and a serine-rich cytoplasmic tail featuring at least 15 potential phosphorylation sites. EPR1 also contains 2 N-linked glycosylation sites, 4 O-linked glycosylation sites, and a chondroitin sulfate attachment site, which may provide anchoring for carbohydrate chains, EPR1 transfectants bind to factor Xa in a specific and saturable manner, and in the absence of factor V/Va promote prothrombin activation in a factor Xa concentration-dependent reaction. Activated platelets and megakaryocytes express EPR1. Both EPR1 and membrane-bound factor Va are thought to be required to mediate factor Xa binding to the activated platelet to form a functional prothrombinase complex.

Supplier: Bioss

Cellular receptors for blood proteases regulate chemotaxis, extracellular proteolysis, and growth behavior of normal and malignant cells. Effector cell protease receptor-1 (EPR1) is a receptor for the coagulation protease factor Xa. EPR1 is characterized by a cysteine-rich extracellular module, a single membrane-spanning domain, and a serine-rich cytoplasmic tail featuring at least 15 potential phosphorylation sites. EPR1 also contains 2 N-linked glycosylation sites, 4 O-linked glycosylation sites, and a chondroitin sulfate attachment site, which may provide anchoring for carbohydrate chains, EPR1 transfectants bind to factor Xa in a specific and saturable manner, and in the absence of factor V/Va promote prothrombin activation in a factor Xa concentration-dependent reaction. Activated platelets and megakaryocytes express EPR1. Both EPR1 and membrane-bound factor Va are thought to be required to mediate factor Xa binding to the activated platelet to form a functional prothrombinase complex.

Supplier: Bioss

HEAT repeats form rod-like helical structures that are involved in intracellular transport. HEATR7B2 (HEAT repeat-containing protein 7B2) is a 1,585 amino acid protein that contains fifteen HEAT repeats. Existing as two alternatively spliced isoforms, the gene encoding HEATR7B2 maps to human chromosome 5p13.1 and mouse chromosome 15 A1. Chromosome 5 contains 181 million base pairs and comprises nearly 6% of the human genome. Cockayne syndrome is associated with chromosome 5 through the ERCC8 gene and familial adenomatous polyposis via the adenomatous polyposis coli (APC) tumor suppressor gene. Treacher Collins syndrome is also chromosome 5-associated and is caused by insertions or deletions within the TCOF1 gene. Deletion of the p arm of chromosome 5 leads to Cri du chat syndrome, while deletion of the q arm or of chromosome 5 altogether is common in therapy-related acute myelogenous leukemias and myelodysplastic syndrome.

Supplier: QUARTZTECHNISCHE WERKSTATTEN

These crucibles and lids are made of quartz glass.

Supplier: Bioss

Members of the Id family of basic helix-loop-helix (bHLH) proteins include Id1 (13), Id2 (4), Id3 and Id4 (5). They are ubiquitously expressed and dimerise with members of the class A and B HLH proteins (15). Due to the absence of the basic region, the resulting heterodimers cannot bind DNA. The Id-type proteins thus appear to negatively regulate DNA binding of bHLH proteins. Since Id1 inhibits DNA binding of E12 and Myo D, it apparently functions to inhibit muscle-specific gene expression. Under conditions that facilitate muscle cell differentiation, the Id protein levels fall, allowing E12 and/or E47 to form heterodimers with Myo D and myogenin, which in turn activate myogenic differentiation. It has been shown that expression of each of the Id proteins is strongly dependent on growth factor activation and that reduction of Id mRNA levels by antisense oligonucleotides leads to a delayed reentry of arrested cells into the cell cycle following growth factor stimulation.

Supplier: Bioss

Cellular receptors for blood proteases regulate chemotaxis, extracellular proteolysis, and growth behavior of normal and malignant cells. Effector cell protease receptor-1 (EPR1) is a receptor for the coagulation protease factor Xa. EPR1 is characterized by a cysteine-rich extracellular module, a single membrane-spanning domain, and a serine-rich cytoplasmic tail featuring at least 15 potential phosphorylation sites. EPR1 also contains 2 N-linked glycosylation sites, 4 O-linked glycosylation sites, and a chondroitin sulfate attachment site, which may provide anchoring for carbohydrate chains, EPR1 transfectants bind to factor Xa in a specific and saturable manner, and in the absence of factor V/Va promote prothrombin activation in a factor Xa concentration-dependent reaction. Activated platelets and megakaryocytes express EPR1. Both EPR1 and membrane-bound factor Va are thought to be required to mediate factor Xa binding to the activated platelet to form a functional prothrombinase complex.

Supplier: MORGAN ADVANCED MATERIALS HALD

These crucibles and lids are made of Alsint 99,7.

Supplier: Bioss

Members of the Id family of basic helix-loop-helix (bHLH) proteins include Id1 (13), Id2 (4), Id3 and Id4 (5). They are ubiquitously expressed and dimerise with members of the class A and B HLH proteins (15). Due to the absence of the basic region, the resulting heterodimers cannot bind DNA. The Id-type proteins thus appear to negatively regulate DNA binding of bHLH proteins. Since Id1 inhibits DNA binding of E12 and Myo D, it apparently functions to inhibit muscle-specific gene expression. Under conditions that facilitate muscle cell differentiation, the Id protein levels fall, allowing E12 and/or E47 to form heterodimers with Myo D and myogenin, which in turn activate myogenic differentiation. It has been shown that expression of each of the Id proteins is strongly dependent on growth factor activation and that reduction of Id mRNA levels by antisense oligonucleotides leads to a delayed reentry of arrested cells into the cell cycle following growth factor stimulation.

Supplier: Bioss

Cellular receptors for blood proteases regulate chemotaxis, extracellular proteolysis, and growth behavior of normal and malignant cells. Effector cell protease receptor-1 (EPR1) is a receptor for the coagulation protease factor Xa. EPR1 is characterized by a cysteine-rich extracellular module, a single membrane-spanning domain, and a serine-rich cytoplasmic tail featuring at least 15 potential phosphorylation sites. EPR1 also contains 2 N-linked glycosylation sites, 4 O-linked glycosylation sites, and a chondroitin sulfate attachment site, which may provide anchoring for carbohydrate chains, EPR1 transfectants bind to factor Xa in a specific and saturable manner, and in the absence of factor V/Va promote prothrombin activation in a factor Xa concentration-dependent reaction. Activated platelets and megakaryocytes express EPR1. Both EPR1 and membrane-bound factor Va are thought to be required to mediate factor Xa binding to the activated platelet to form a functional prothrombinase complex.

Supplier: Bioss

Cellular receptors for blood proteases regulate chemotaxis, extracellular proteolysis, and growth behavior of normal and malignant cells. Effector cell protease receptor-1 (EPR1) is a receptor for the coagulation protease factor Xa. EPR1 is characterized by a cysteine-rich extracellular module, a single membrane-spanning domain, and a serine-rich cytoplasmic tail featuring at least 15 potential phosphorylation sites. EPR1 also contains 2 N-linked glycosylation sites, 4 O-linked glycosylation sites, and a chondroitin sulfate attachment site, which may provide anchoring for carbohydrate chains, EPR1 transfectants bind to factor Xa in a specific and saturable manner, and in the absence of factor V/Va promote prothrombin activation in a factor Xa concentration-dependent reaction. Activated platelets and megakaryocytes express EPR1. Both EPR1 and membrane-bound factor Va are thought to be required to mediate factor Xa binding to the activated platelet to form a functional prothrombinase complex.