You Searched For: COVID+sign

Catalog Number: (89416-054)

Supplier: Prosci

Description: Pst1 Antibody: Protoplast secreted protein 1 (Pst1) is an anchored plasma membrane protein. Pst1 was previously identified as a protein secreted by yeast regenerating protoplasts, which suggests a role in cell wall construction. Pst1 is a protein with 444 amino acids and is attached to yeast cell wall via a glycosylphosphatidylinisotol (GPI) anchor. Pst1 contains 15 potential N-linked glycosylation sites and is heavily glycosylated. It migrates at approximately 200 kDa on SDS-PAGE when produced in wild type S. cerevisiae. Our Pst1 protein (Catalog No. 95-151) was expressed in a genetically manipulated triple-mutant (TM) S. cerevisiae stain ( Delta och1 Delta mnn1 Delta mnn4), which results in the production of sole Man8GlcNAc2 carbohydrate structures and Pst1 migration at approximately 100 kDa. When produced in the TM yeast, Pst1 can be recognized by several glycan-specific HIV-1 broadly neutralizing antibodies, including 2G12 and recently identified PGT antibodies. Among several heavily N-glycosylated TM yeast glycoproteins, Pst1 shows higher affinity for 2G12 and efficiently inhibits gp120 interactions with 2G12 and DC-SIGN, and it also blocks 2G12-mediated neutralization of HIV-1 pseudoviruses.

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Catalog Number: (10476-152)

Supplier: Bioss

Description: May be a chaperone-like protein essential for the proper conformation and functioning of protein complexes in the respiratory chain.Tissue specificity:Ubiquitously expressed with a relatively greater abundance in heart and skeletal muscle.Involvement in disease:Defects in ADCK3 are a cause of coenzyme Q10 deficiency (CoQ10 deficiency). CoQ10 deficiency is an autosomal recessive disorder with variable manifestations. It can be associated with three main clinical phenotypes: a predominantly myopathic form with central nervous system involvement, an infantile encephalomyopathy with renal dysfunction and an ataxic form with cerebellar atrophy.Defects in ADCK3 are the cause of spinocerebellar ataxia autosomal recessive type 9 (SCAR9) [MIM:612016]; also known as autosomal recessive cerebellar ataxia type 2 (ARCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCAR9 is an autosomal recessive form characterized by gait ataxia and cerebellar atrophy with slow progression and few associated features. Patients can manifest brisk tendon reflexes and Hoffmann sign, mild psychomotor retardation, mild axonal degeneration of the sural nerve, exercise intolerance and elevated serum lactate.

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Catalog Number: (10476-140)

Supplier: Bioss

Description: May be a chaperone-like protein essential for the proper conformation and functioning of protein complexes in the respiratory chain.Tissue specificity:Ubiquitously expressed with a relatively greater abundance in heart and skeletal muscle.Involvement in disease:Defects in ADCK3 are a cause of coenzyme Q10 deficiency (CoQ10 deficiency). CoQ10 deficiency is an autosomal recessive disorder with variable manifestations. It can be associated with three main clinical phenotypes: a predominantly myopathic form with central nervous system involvement, an infantile encephalomyopathy with renal dysfunction and an ataxic form with cerebellar atrophy.Defects in ADCK3 are the cause of spinocerebellar ataxia autosomal recessive type 9 (SCAR9) [MIM:612016]; also known as autosomal recessive cerebellar ataxia type 2 (ARCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCAR9 is an autosomal recessive form characterized by gait ataxia and cerebellar atrophy with slow progression and few associated features. Patients can manifest brisk tendon reflexes and Hoffmann sign, mild psychomotor retardation, mild axonal degeneration of the sural nerve, exercise intolerance and elevated serum lactate.

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Catalog Number: (10481-994)

Supplier: Bioss

Description: 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.

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Catalog Number: (10291-614)

Supplier: Bioss

Description: C16orf63, also known as FLJ31153 or DKFZp686N1651, is a 174 amino acid protein that contains one LisH domain. The gene that encodes C16orf63 maps to human chromosome 16. Chromosome 16 encodes over 900 genes in approximately 90 million base pairs, makes up nearly 3% of human cellular DNA and is associated with a variety of genetic disorders. The GAN gene is located on chromosome 16 and, with mutation, may lead to giant axonal neuropathy, a nervous system disorder characterized by increasing malfunction with growth. The rare disorder Rubinstein-Taybi syndrome is also associated with chromosome 16, though through the CREBBP gene which encodes a critical CREB binding protein. Signs of Rubinstein-Taybi include mental retardation and predisposition to tumor growth and white blood cell neoplasias. Crohn's disease is a gastrointestinal inflammatory condition associated with chromosome 16 through the NOD2 gene. An association with systemic lupus erythematosis and a number of other autoimmune disorders with the pericentromeric region of chromosome 16 has led to the identification of SLC5A11 as a potential autoimmune modifier. The C16orf63 gene product has been provisionally designated C16orf63 pending further characterization.

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Catalog Number: (10291-612)

Supplier: Bioss

Description: C16orf63, also known as FLJ31153 or DKFZp686N1651, is a 174 amino acid protein that contains one LisH domain. The gene that encodes C16orf63 maps to human chromosome 16. Chromosome 16 encodes over 900 genes in approximately 90 million base pairs, makes up nearly 3% of human cellular DNA and is associated with a variety of genetic disorders. The GAN gene is located on chromosome 16 and, with mutation, may lead to giant axonal neuropathy, a nervous system disorder characterized by increasing malfunction with growth. The rare disorder Rubinstein-Taybi syndrome is also associated with chromosome 16, though through the CREBBP gene which encodes a critical CREB binding protein. Signs of Rubinstein-Taybi include mental retardation and predisposition to tumor growth and white blood cell neoplasias. Crohn's disease is a gastrointestinal inflammatory condition associated with chromosome 16 through the NOD2 gene. An association with systemic lupus erythematosis and a number of other autoimmune disorders with the pericentromeric region of chromosome 16 has led to the identification of SLC5A11 as a potential autoimmune modifier. The C16orf63 gene product has been provisionally designated C16orf63 pending further characterization.

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Catalog Number: (76119-344)

Supplier: Bioss

Description: Chromosome 16 encodes over 900 genes in approximately 90 million base pairs, makes up nearly 3% of human cellular DNA and is associated with a variety of genetic disorders. The GAN gene is located on chromosome 16 and, with mutation, may lead to giant axonal neuropathy, a nervous system disorder characterized by increasing malfunction with growth. The rare disorder Rubinstein-Taybi syndrome is also associated with chromosome 16, though through the CREBBP gene which encodes a critical CREB binding protein. Signs of Rubinstein-Taybi include mental retardation and predisposition to tumor growth and white blood cell neoplasias. Crohn's disease is a gastrointestinal inflammatory condition associated with chromosome 16 through the NOD2 gene. An association with systemic lupus erythematosis and a number of other autoimmune disorders with the pericentromeric region of chromosome 16 has led to the identification of SLC5A11 as a potential autoimmune modifier. The C16orf72 gene product has been provisionally designated C16orf72 pending further characterization.

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Supplier: Biotium

Description: This antibody recognizes the epsilon-chain of CD3, which consists of five different polypeptide chains (designated as gamma, delta, epsilon, zeta, and eta) with MW ranging from 16-28 kDa. The CD3 complex is closely associated at the lymphocyte cell surface with the T cell antigen receptor (TCR). Reportedly, CD3 complex is involved in signal transduction to the T cell interior following antigen recognition. The CD3 antigen is first detectable in early thymocytes and probably represents one of the earliest signs of commitment to the T cell lineage. In cortical thymocytes, CD3 is predominantly intra-cytoplasmic. However, in medullary thymocytes, it appears on the T cell surface. CD3 antigen is a highly specific marker for T cells, and is present in majority of T cell neoplasms.

CF® dyes are Biotium's next-generation fluorescent dyes. CF®488A is a green fluorescent dye (Ex/Em 490/515 nm) with excellent brightness and photostability. The dye is minimally charged for less non-specific binding. CF®488A also is compatible with super-resolution imaging by TIRF.

Catalog Number: (10278-406)

Supplier: Bioss

Description: ZNF843 is a 348 amino acid protein that is encoded by a gene which maps to chromosome 16. Chromosome 16 encodes over 900 genes in approximately 90 million base pairs, makes up nearly 3% of human cellular DNA and is associated with a variety of genetic disorders. The GAN gene is located on chromosome 16 and, with mutation, may lead to giant axonal neuropathy, a nervous system disorder characterized by increasing malfunction with growth. The rare disorder Rubinstein-Taybi syndrome is also associated with chromosome 16 through the CREBBP gene which encodes a critical CREB binding protein. Signs of Rubinstein-Taybi include mental retardation and predisposition to tumor growth and white blood cell neoplasias. Crohn's disease is a gastrointestinal inflammatory condition associated with chromosome 16 through the NOD2 gene. An association with systemic lupus erythematosis and a number of other autoimmune disorders with the pericentromeric region of chromosome 16 has led to the identification of SLC5A11 as a potential autoimmune modifier. The ZNF843 gene product has been provisionally designated MGC46336 pending further characterization.

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Catalog Number: (10482-240)

Supplier: Bioss

Description: 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.

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Supplier: WaterSaver Faucet

Description: Designed to provide complete personal protection, these corrosion-resistant safety stations feature a single water inlet that supplies both the shower and eye wash.

Catalog Number: (76108-216)

Supplier: Bioss

Description: May be a chaperone-like protein essential for the proper conformation and functioning of protein complexes in the respiratory chain.Tissue specificity:Ubiquitously expressed with a relatively greater abundance in heart and skeletal muscle.Involvement in disease:Defects in ADCK3 are a cause of coenzyme Q10 deficiency (CoQ10 deficiency). CoQ10 deficiency is an autosomal recessive disorder with variable manifestations. It can be associated with three main clinical phenotypes: a predominantly myopathic form with central nervous system involvement, an infantile encephalomyopathy with renal dysfunction and an ataxic form with cerebellar atrophy.Defects in ADCK3 are the cause of spinocerebellar ataxia autosomal recessive type 9 (SCAR9) [MIM:612016]; also known as autosomal recessive cerebellar ataxia type 2 (ARCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCAR9 is an autosomal recessive form characterized by gait ataxia and cerebellar atrophy with slow progression and few associated features. Patients can manifest brisk tendon reflexes and Hoffmann sign, mild psychomotor retardation, mild axonal degeneration of the sural nerve, exercise intolerance and elevated serum lactate.

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Catalog Number: (76108-214)

Supplier: Bioss

Description: May be a chaperone-like protein essential for the proper conformation and functioning of protein complexes in the respiratory chain.Tissue specificity:Ubiquitously expressed with a relatively greater abundance in heart and skeletal muscle.Involvement in disease:Defects in ADCK3 are a cause of coenzyme Q10 deficiency (CoQ10 deficiency). CoQ10 deficiency is an autosomal recessive disorder with variable manifestations. It can be associated with three main clinical phenotypes: a predominantly myopathic form with central nervous system involvement, an infantile encephalomyopathy with renal dysfunction and an ataxic form with cerebellar atrophy.Defects in ADCK3 are the cause of spinocerebellar ataxia autosomal recessive type 9 (SCAR9) [MIM:612016]; also known as autosomal recessive cerebellar ataxia type 2 (ARCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCAR9 is an autosomal recessive form characterized by gait ataxia and cerebellar atrophy with slow progression and few associated features. Patients can manifest brisk tendon reflexes and Hoffmann sign, mild psychomotor retardation, mild axonal degeneration of the sural nerve, exercise intolerance and elevated serum lactate.

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Catalog Number: (10291-616)

Supplier: Bioss

Description: C16orf63, also known as FLJ31153 or DKFZp686N1651, is a 174 amino acid protein that contains one LisH domain. The gene that encodes C16orf63 maps to human chromosome 16. Chromosome 16 encodes over 900 genes in approximately 90 million base pairs, makes up nearly 3% of human cellular DNA and is associated with a variety of genetic disorders. The GAN gene is located on chromosome 16 and, with mutation, may lead to giant axonal neuropathy, a nervous system disorder characterized by increasing malfunction with growth. The rare disorder Rubinstein-Taybi syndrome is also associated with chromosome 16, though through the CREBBP gene which encodes a critical CREB binding protein. Signs of Rubinstein-Taybi include mental retardation and predisposition to tumor growth and white blood cell neoplasias. Crohn's disease is a gastrointestinal inflammatory condition associated with chromosome 16 through the NOD2 gene. An association with systemic lupus erythematosis and a number of other autoimmune disorders with the pericentromeric region of chromosome 16 has led to the identification of SLC5A11 as a potential autoimmune modifier. The C16orf63 gene product has been provisionally designated C16orf63 pending further characterization.

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Catalog Number: (10476-162)

Supplier: Bioss

Description: May be a chaperone-like protein essential for the proper conformation and functioning of protein complexes in the respiratory chain.Tissue specificity:Ubiquitously expressed with a relatively greater abundance in heart and skeletal muscle.Involvement in disease:Defects in ADCK3 are a cause of coenzyme Q10 deficiency (CoQ10 deficiency). CoQ10 deficiency is an autosomal recessive disorder with variable manifestations. It can be associated with three main clinical phenotypes: a predominantly myopathic form with central nervous system involvement, an infantile encephalomyopathy with renal dysfunction and an ataxic form with cerebellar atrophy.Defects in ADCK3 are the cause of spinocerebellar ataxia autosomal recessive type 9 (SCAR9) [MIM:612016]; also known as autosomal recessive cerebellar ataxia type 2 (ARCA2). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCAR9 is an autosomal recessive form characterized by gait ataxia and cerebellar atrophy with slow progression and few associated features. Patients can manifest brisk tendon reflexes and Hoffmann sign, mild psychomotor retardation, mild axonal degeneration of the sural nerve, exercise intolerance and elevated serum lactate.

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Supplier: Eagle Manufacturing

Description: Cabinets are constructed of tough, double-walled 18-gauge steel with 3.8 cm (1½") air space between walls.