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This Item | 565788 | 565780 | 565749 |
|---|---|---|---|
| form powder | form solid | form lyophilized | form solid |
| assay ≥97% (HPLC) | assay ≥98% (HPLC) | assay ≥95% (HPLC) | assay ≥95% (HPLC) |
| Quality Level 200 | Quality Level 100 | Quality Level 100 | Quality Level 100 |
| mol wt ~_1.65 kDa | mol wt - | mol wt - | mol wt - |
| storage temp. −20°C | storage temp. 2-8°C | storage temp. −20°C | storage temp. −20°C |
| solubility DMSO: soluble | solubility DMSO: 100 mg/mL | solubility DMSO: 1 mg/mL | solubility DMSO: 5 mg/mL |
General description
This gene encodes a membrane glycoprotein of T lymphocytes that interacts with major histocompatibility complex class II antigenes and is also a receptor for the human immunodeficiency virus. This gene is expressed not only in T lymphocytes, but also in B cells, macrophages, and granulocytes. It is also expressed in specific regions of the brain. The protein functions to initiate or augment the early phase of T-cell activation, and may function as an important mediator of indirect neuronal damage in infectious and immune-mediated diseases of the central nervous system. Multiple alternatively spliced transcript variants encoding different isoforms have been identified in this gene. [provided by RefSeq, Aug 2010]
Immunogen
A synthesized peptide derived from human CD4
Physical form
Buffer: PBS with 0.02% sodium azide,0.05% BSA,50% glycerol,pH7.3.
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Storage Class
12 - Non Combustible Liquids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
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Jungmi Lee et al.
Analytica chimica acta, 1022, 89-95 (2018-05-08)
Amyloid-β (Aβ) is generated by proteolytic processing of amyloid precursor protein (APP) by beta-secretase (BACE-1) and gamma-secretase. Amyloid-β is responsible for the formation of senile plaques in Alzheimer's disease (AD). Consequently, inhibition of β-secretase (BACE-1), a rate-limiting enzyme in the
Hans Hilpert et al.
Journal of medicinal chemistry, 56(10), 3980-3995 (2013-04-18)
An extensive fluorine scan of 1,3-oxazines revealed the power of fluorine(s) to lower the pKa and thereby dramatically change the pharmacological profile of this class of BACE1 inhibitors. The CF3 substituted oxazine 89, a potent and highly brain penetrant BACE1
beta-secretase inhibitor; a promising novel therapeutic drug in Alzheimer?s disease
Menting KW, et al.
Frontiers in Aging Neuroscience, 6, 165-165 (2014)
S Sinha et al.
Nature, 402(6761), 537-540 (1999-12-11)
Proteolytic processing of the amyloid precursor protein (APP) generates amyloid beta (Abeta) peptide, which is thought to be causal for the pathology and subsequent cognitive decline in Alzheimer's disease. Cleavage by beta-secretase at the amino terminus of the Abeta peptide
Patty C Kandalepas et al.
Acta neuropathologica, 126(3), 329-352 (2013-07-04)
β-Site amyloid precursor protein (APP) cleaving enzyme-1 (BACE1) is the β-secretase that initiates Aβ production in Alzheimer's disease (AD). BACE1 levels are increased in AD, which could contribute to pathogenesis, yet the mechanism of BACE1 elevation is unclear. Furthermore, the
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