脂质 (Lipid) 是中性脂肪、类脂及其衍生物的总称，其共同的物理特性是不溶于水，易溶于有机溶剂(如乙醇、乙醚等)。人体的脂肪主要有两种

1、储存脂肪，如中性脂肪，主要分布于皮下、肾、胰腺等部位。

2、结构脂肪，如类脂 (磷脂、糖脂、胆固醇等)，主要分布于细胞内。中性脂肪 (Neutral fat) 是由三分子脂肪酸和一分子甘油组成的脂类，呈中性。中性脂肪染色经常采用苏丹Ⅱ、苏丹Ⅲ、苏丹Ⅳ、苏丹黑B、油红O法等。传统方法采用苏丹染料，最近发现偶氮染料油红O更适合脂肪的染色。油红O是很强的脂溶剂和染脂剂，较易与甘油三脂结合呈小脂滴状，与磷脂结合力稍差，其染色原理一般认为是物理上的溶液作用或吸附作用，借溶液作用使脂肪染色。 

油红O染色试剂盒 (细胞专用) 主要用于显示人工培养细胞的脂肪变性和类脂质的异常沉着，细胞内出现多数中性脂肪滴，鉴别培养细胞中所发生的变化及其性质。标本不采用含有乙醇的固定液，脂肪的阳性染色结果呈橘黄至红色，但具体颜色因脂质浓度而定。 

本产品仅用于科研领域，不用于临床诊断。

Function:
Cytokine with a wide variety of biological functions. It is a potent inducer of the acute phase response. Plays an essential role in the final differentiation of B-cells into Ig-secreting cells Involved in lymphocyte and monocyte differentiation. It induces myeloma and plasmacytoma growth and induces nerve cells differentiation Acts on B-cells, T-cells, hepatocytes, hematopoietic progenitor cells and cells of the CNS. Also acts as a myokine. It is discharged into the bloodstream after muscle contraction and acts to increase the breakdown of fats and to improve insulin resistance.

Subcellular Location:
Secreted.

Post-translational modifications:
N- and O-glycosylated.

DISEASE:
Genetic variations in IL6 are associated with susceptibility to rheumatoid arthritis systemic juvenile (RASJ) [MIM:604302]. An inflammatory articular disorder with systemic-onset beginning before the age of 16. It represents a subgroup of juvenile arthritis associated with severe extraarticular features and occasionally fatal complications. During active phases of the disorder, patients display a typical daily spiking fever, an evanescent macular rash, lymphadenopathy, hepatosplenomegaly, serositis, myalgia and arthritis.
Note=A IL6 promoter polymorphism is associated with a lifetime risk of development of Kaposi sarcoma in HIV-infected men.

Similarity:
Belongs to the IL-6 superfamily.

SWISS:
P05231

Gene ID:
3569

Database links:

Entrez Gene: 3569 Human

Entrez Gene: 16193 Mouse

Entrez Gene: 24498 Rat

Omim: 147620 Human

SwissProt: P05231 Human

SwissProt: P08505 Mouse

SwissProt: P20607 Rat

Unigene: 654458 Human

Unigene: 1019 Mouse

Unigene: 9873 Rat

SWISS:
P0DTC9

Gene ID:
43740575

Function:
Functions as a master transcriptional regulator of theadaptive response to hypoxia. Under hypoxic conditions activatesthe transcription of over 40 genes, including, erythropoietin,glucose transporters, glycolytic enzymes, vascular endothelialgrowth factor, and other genes whose protein products increaseoxygen delivery or facilitate metabolic adaptation to hypoxia.Plays an essential role in embryonic vascularization, tumorangiogenesis and pathophysiology of ischemic disease. Binds to coreDNA sequence 5′-[AG]CGTG-3′ within the hypoxia response element(HRE) of target gene promoters. Activation requires recruitment oftranscriptional coactivators such as CREBPB and EP300. Activity isenhanced by interaction with both, NCOA1 or NCOA2. Interaction withredox regulatory protein APEX seems to activate CTAD andpotentiates activation by NCOA1 and CREBBP.

Subunit:
Interacts with COPS5 subunit of COP9 signalosome complex,leading to the regulation of its stability. Interacts with TSGA10(By similarity). Efficient DNA binding requires heterodimerizationof an alpha and a beta/ARNT subunit. Binds to the TAZ-type 1domains of CREBBP and EP300. Interacts with NCOA1, NCOA2, APEX andHSP90. Interacts with VHL which docks HFA1 to the E3 ubiquitinligase complex for subsequent destruction. Interaction, via the ODDdomain, with the beta domain of VHLL, protects HIF1A fromdestruction by competing against the destructive targetinginitiated by VHL.

Subcellular Location:
Cytoplasm. Nucleus.

Tissue Specificity:
Expressed in most tissues with highest levels in kidney and heart. Overexpressed in the majority of common human cancers and their metastases, due to the presence of intratumoral hypoxia and as a result of mutations in genes encoding oncoproteins and tumor suppressors.

Post-translational modifications:
In normoxia, is hydroxylated on Pro-402 and Pro-564 in theoxygen-dependent degradation domain (ODD) by EGLN1/PHD1 andEGLN2/PHD2. EGLN3/PHD3 has also been shown to hydroxylate Pro-564.The hydroxylated prolines promote interaction with VHL, initiatingrapid ubiquitination and subsequent proteasomal degradation. Underhypoxia, proline hydroxylation is impaired and ubiquitination isattenuated, resulting in stabilization.
In normoxia, is hydroxylated on Asn-803 by HIF1AN, thusabrogating interaction with CREBBP and EP300 and preventingtranscriptional activation.
S-nitrosylation of Cys-800 may be responsible for increasedrecruitment of p300 coactivator necessary for transcriptionalactivity of HIF-1 complex.
Acetylation of Lys-532 by ARD1 increases interaction with VHLand stimulates subsequent proteasomal degradation.
Requires phosphorylation for DNA-binding.

Similarity:
Contains 1 basic helix-loop-helix (bHLH) domain.
Contains 1 PAC (PAS-associated C-terminal) domain.
Contains 2 PAS (PER-ARNT-SIM) domains.

SWISS:
Q16665

Gene ID:
3091

Database links:

Entrez Gene: 3091 Human

Entrez Gene: 15251 Mouse

Omim: 603348 Human

SwissProt: Q16665 Human

SwissProt: Q61221 Mouse

Unigene: 597216 Human

Unigene: 3879 Mouse

Unigene: 446610 Mouse

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

缺氧诱导因子1α不仅对于机体在缺氧条件下维持正常的生理功能具有特别重要的意义,并在肿瘤的生长以及神经细胞凋亡等病理过程中起重要作用. HIF1 alpha能调节许多下游基因的表达水平.
哺乳动物细胞在低氧压力条件下出现HIF。HIF是一种转录因子，对细胞的缺氧起稳定作用。

Function:
Type II collagen is specific for cartilaginous tissues. It is essential for the normal embryonic development of the skeleton, for linear growth and for the ability of cartilage to resist compressive forces.

Subunit:
Homotrimers of alpha 1(II) chains.

Subcellular Location:
Secreted, extracellular space, extracellular matrix.

Tissue Specificity:
Isoform 2 is highly expressed in juvenile chondrocyte and low in fetal chondrocyte.

Post-translational modifications:
Probably 3-hydroxylated on prolines by LEPREL1 (By similarity). Proline residues at the third position of the tripeptide repeating unit (G-X-P) are hydroxylated in some or all of the chains. Proline residues at the second position of the tripeptide repeating unit (G-P-X) are hydroxylated in some of the chains.
The N-telopeptide is covalently linked to the helical COL2 region of alpha 1(IX), alpha 2(IX) and alpha 3(IX) chain. The C-telopeptide is covalently linked to an another site in the helical region of alpha 3(IX) COL2.

DISEASE:
Defects in COL2A1 are the cause of spondyloepiphyseal dysplasia congenital type (SEDC) [MIM:183900]. This disorder is characterized by disproportionate short stature and pleiotropic involvement of the skeletal and ocular systems.
Defects in COL2A1 are the cause of spondyloepimetaphyseal dysplasia Strudwick type (SEMJP-STR) [MIM:184250]. A bone disease characterized by disproportionate short stature from birth, with a very short trunk and shortened limbs, and skeletal abnormalities including lordosis, scoliosis, flattened vertebrae, pectus carinatum, coxa vara, clubfoot, and abnormal epiphyses or metaphyses. A distinctive radiographic feature is irregular sclerotic changes, described as dappled in the metaphyses of the long bones.
Defects in COL2A1 are the cause of achondrogenesis type 2 (ACG2) [MIM:200610]; also known as achondrogenesis-hypochondrogenesis type II. ACG2 is a disease characterized by the absence of ossification in the vertebral column, sacrum and pubic bones.
Defects in COL2A1 are the cause of Legg-Calve-Perthes disease (LCPD) [MIM:150600]; also known as Legg-Perthes disease or Perthes disease. LCPD is characterized by loss of circulation to the femoral head, resulting in avascular necrosis in a growing child. Clinical pictures of the disease vary, depending on the phase of disease progression through ischemia, revascularization, fracture and collapse, and repair and remodeling of the bone.
Defects in COL2A1 are the cause of Kniest dysplasia (KD) [MIM:156550]; also known as Kniest syndrome or metatropic dwarfism type II. KD is a moderately severe chondrodysplasia phenotype that results from mutations in the COL2A1 gene. Characteristics of the disorder include a short trunk and extremities, mid-face hypoplasia, cleft palate, myopia, retinal detachment, and hearing loss.
Defects in COL2A1 are a cause of primary avascular necrosis of femoral head (ANFH) [MIM:608805]; also known as ischemic necrosis of the femoral head or osteonecrosis of the femoral head. ANFH causes disability that often requires surgical intervention. Most cases are sporadic, but families in which there is an autosomal dominant inheritance of the disease have been identified. It has been estimated that 300,000 to 600,000 people in the United States have ANFH. Approximately 15,000 new cases of this common and disabling disorder are reported annually. The age at the onset is earlier than that for osteoarthritis. The diagnosis is typically made when patients are between the ages of 30 and 60 years. The clinical manifestations, such as pain on exertion, a limping gait, and a discrepancy in leg length, cause considerable disability. Moreover, nearly 10 percent of the 500,000 total-hip arthroplasties performed each year in the United States involve patients with ANFH. As a result, this disease creates a substantial socioeconomic cost as well as a burden for patients and their families.
Defects in COL2A1 are the cause of osteoarthritis with mild chondrodysplasia (OACD) [MIM:604864]. Osteoarthritis is a common disease that produces joint pain and stiffness together with radiologic evidence of progressive degeneration of joint cartilage. Some forms of osteoarthritis are secondary to events such as trauma, infections, metabolic disorders, or congenital or heritable conditions that deform the epiphyses or related structures. In most patients, however, there is no readily identifiable cause of osteoarthritis. Inheritance in a Mendelian dominant manner has been demonstrated in some families with primary generalized osteoarthritis. Reports demonstrate coinheritance of primary generalized osteoarthritis with specific alleles of the gene COL2A1, the precursor of the major protein of cartilage.
Defects in COL2A1 are the cause of platyspondylic lethal skeletal dysplasia Torrance type (PLSJP-T) [MIM:151210]. Platyspondylic lethal skeletal dysplasias (PLSDs) are a heterogeneous group of chondrodysplasias characterized by severe platyspondyly and limb shortening. PLSJP-T is characterized by varying platyspondyly, short ribs with anterior cupping, hypoplasia of the lower ilia with broad ischial and pubic bones, and shortening of the tubular bones with splayed and cupped metaphyses. Histology of the growth plate typically shows focal hypercellularity with slightly enlarged chondrocytes in the resting cartilage and relatively well-preserved columnar formation and ossification at the chondro-osseous junction. PLSJP-T is generally a perinatally lethal disease, but a few long-term survivors have been reported.
Defects in COL2A1 are the cause of multiple epiphyseal dysplasia with myopia and conductive deafness (EDMMD) [MIM:132450]. Multiple epiphyseal dysplasia is a generalized skeletal dysplasia associated with significant morbidity. Joint pain, joint deformity, waddling gait, and short stature are the main clinical signs and symptoms. EDMMD is an autosomal dominant disorder characterized by epiphyseal dysplasia associated with progressive myopia, retinal thinning, crenated cataracts, conductive deafness.
Defects in COL2A1 are the cause of spondyloperipheral dysplasia (SPD) [MIM:271700]. SPD patients manifest short stature, midface hypoplasia, sensorineural hearing loss, spondyloepiphyseal dysplasia, platyspondyly and brachydactyly.

Similarity:
Belongs to the fibrillar collagen family.
Contains 1 fibrillar collagen NC1 domain.
Contains 1 VWFC domain.

SWISS:
P02458

Gene ID:
1280

Database links:

Entrez Gene: 1280 Human

Entrez Gene: 12824 Mouse

Entrez Gene: 25412 Rat

Omim: 120140 Human

SwissProt: P02458 Human

SwissProt: P28481 Mouse

SwissProt: P05539 Rat

Unigene: 408182 Human

Unigene: 2423 Mouse

Unigene: 10124 Rat

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

Function:
Has both glyceraldehyde-3-phosphate dehydrogenase and nitrosylase activities, thereby playing a role in glycolysis and nuclear functions, respectively. Participates in nuclear events including transcription, RNA transport, DNA replication and apoptosis. Nuclear functions are probably due to the nitrosylase activity that mediates cysteine S-nitrosylation of nuclear target proteins such as SIRT1, HDAC2 and PRKDC. Glyceraldehyde-3-phosphate dehydrogenase is a key enzyme in glycolysis that catalyzes the first step of the pathway by converting JP-glyceraldehyde 3-phosphate (G3P) into 3-phospho-JP-glyceroyl phosphate.

Subunit:
Homotetramer. Interacts with TPPP; the interaction is direct. Interacts (when S-nitrosylated) with SIAH1; leading to nuclear translocation. Interacts with RILPL1/GOSPEL, leading to prevent the interaction between GAPDH and SIAH1 and prevent nuclear translocation. Interacts with EIF1AD, USP25, PRKCI and WARS.

Subcellular Location:
Cytoplasm, cytosol. Nucleus. Cytoplasm, perinuclear region. Membrane. Note=Translocates to the nucleus following S-nitrosylation and interaction with SIAH1, which contains a nuclear localization signal. Postnuclear and Perinuclear regions.

Post-translational modifications:
S-nitrosylation of Cys-152 leads to interaction with SIAH1, followed by translocation to the nucleus.
ISGylated (Probable).
Sulfhydration at Cys-152 increases catalytic activity.

Similarity:
Belongs to the glyceraldehyde-3-phosphate dehydrogenase family.

SWISS:
P04406

Gene ID:
100009074

Database links:

Entrez Gene: 493876 Cat

Entrez Gene: 374193 Chicken

Entrez Gene: 403755 Dog

Entrez Gene: 2597 Human

Entrez Gene: 100042025 Mouse

Entrez Gene: 14433 Mouse

Entrez Gene: 396823 Pig

Entrez Gene: 100009074 Rabbit

Entrez Gene: 24383 Rat

Entrez Gene: 685186 Rat

Entrez Gene: 380259 Xenopus laevis

Entrez Gene: 448356 Xenopus tropicalis

Entrez Gene: 317743 Zebrafish

Omim: 138400 Human

SwissProt: Cat

SwissProt: P00356 Chicken

SwissProt: Q28259 Dog

SwissProt: P70685 Guinea pig

SwissProt: P04406 Human

SwissProt: P16858 Mouse

SwissProt: P00355 Pig

SwissProt: P46406 Rabbit

SwissProt: P04797 Rat

SwissProt: P51469 Xenopus laevis

SwissProt: Q5XJ10 Zebrafish

Unigene: 544577 Human

Unigene: 592355 Human

Unigene: 598320 Human

Unigene: 304088 Mouse

Unigene: 309092 Mouse

Unigene: 317779 Mouse

Unigene: 343110 Mouse

Unigene: 392463 Mouse

Unigene: 392480 Mouse

Unigene: 414470 Mouse

Unigene: 458138 Mouse

Unigene: 458416 Mouse

Unigene: 475698 Mouse

Unigene: 129558 Rat

Unigene: 91450 Rat

Unigene: 995 Xenopus laevis

Unigene: 35640 Zebrafish

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

甘油醛-3-磷酸脱氢酶（Glyceraldehyde 3 phosphate dehydrogenase，GAPDH）是糖酵解（glycolysis）过程中的关键酶。除了在胞质中作为糖酵解的酶以外，有证据表明哺乳动物细胞中的GAPDH参与了多种胞内生化过程，包括膜融合（membrane fusion）、微管成束（microtubule bundling）、磷酸转移酶（phosphotransferase）激活、核内RNA出核、DNA复制与DNA修复。一些生理因素，诸如低氧（hypoxia）和尿糖（diabetes），可以增加GAPDH在特定细胞中的表达。GAPDH存在于几乎所有的组织中，以高水平持续表达。 GAPDH（甘油醛-3-磷酸脱氢酶）是参与糖酵解的一种关键酶，由4个30－40kDa的亚基组成。

  为应对 COVIJP-19疫情的爆发，北京博奥森生物技术有限公司启动了针对新型冠状病毒的科研攻关，成功研发出SARS-CoV-2 (2019-nCoV) Nucleoprotein蛋白检测试剂盒。  该试剂盒根据ELISA双抗体夹心法原理，采用一步法，实现对2019-nCoV抗原蛋白的快速准确检测。试剂盒所采用原料均来自本公司科研团队自主研发，经严苛筛选验证，保证其灵敏度高、特异性好，结果一致且可靠，为疫情的相关疫苗及治疗性药物研究等工作贡献一份力量。

产品特色：
1 时间短，提高检测效率；
2 操作简便，实验误差更小；
3 样本需求量小，节约珍贵检测样本；
4 灵敏度高及特异性好，结果一致且可靠。

Function:
Involved in the activation cascade of caspases responsible for apoptosis execution. At the onset of apoptosis it proteolytically cleaves poly(ADP-ribose) polymerase (PARP) at a ‘216-Asp-|-Gly-217’ bond. Cleaves and activates sterol regulatory element binding proteins (SREBPs) between the basic helix-loop-helix leucine zipper domain and the membrane attachment domain. Cleaves and activates caspase-6, -7 and -9. Involved in the cleavage of huntingtin. Triggers cell adhesion in sympathetic neurons through RET cleavage.

Subunit:
Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 17 kDa (p17) and a 12 kDa (p12) subunit. Interacts with BIRC6/bruce.

Subcellular Location:
Cytoplasm.

Tissue Specificity:
Highly expressed in lung, spleen, heart, liver and kidney. Moderate levels in brain and skeletal muscle, and low in testis. Also found in many cell lines, highest expression in cells of the immune system.

Post-translational modifications:
Cleavage by granzyme B, caspase-6, caspase-8 and caspase-10 generates the two active subunits. Additional processing of the propeptides is likely due to the autocatalytic activity of the activated protease. Active heterodimers between the small subunit of caspase-7 protease and the large subunit of caspase-3 also occur and vice versa.
S-nitrosylated on its catalytic site cysteine in unstimulated human cell lines and denitrosylated upon activation of the Fas apoptotic pathway, associated with an increase in intracellular caspase activity. Fas therefore activates caspase-3 not only by inducing the cleavage of the caspase zymogen to its active subunits, but also by stimulating the denitrosylation of its active site thiol.

Similarity:
Belongs to the peptidase C14A family.

SWISS:
P42574

Gene ID:
836

Database links:

Entrez Gene: 836 Human

Entrez Gene: 12367 Mouse

Entrez Gene: 397244 Pig

Entrez Gene: 100008840 Rabbit

Entrez Gene: 25402 Rat

Omim: 600636 Human

SwissProt: P42574 Human

SwissProt: P70677 Mouse

SwissProt: Q95ND5 Pig

SwissProt: Q8MJC3 Rabbit

SwissProt: P55213 Rat

Unigene: 141125 Human

Unigene: 34405 Mouse

Unigene: 10562 Rat

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

Caspase3广泛分布于各种不同类型的细胞中，是Caspase家族中最重要的凋亡执行者之一，激活的Caspase-3能使许多与细胞结构、细胞周期及DNA修复等相关蛋白或激酶失活，从而使细胞凋亡.

Function:
Transcription factor involved in osteoblastic differentiation and skeletal morphogenesis. Essential for the maturation of osteoblasts and both intramembranous and endochondral ossification. CBF binds to the core site, 5′-PYGPYGGT-3′, of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers, osteocalcin, osteopontin, bone sialoprotein, alpha 1(I) collagen, LCK, IL-3 and GM-CSF promoters (By similarity). Inhibits MYST4-dependent transcriptional activation. [SUBUNIT] Interaction with SATB2 results in enhanced DNA binding and transactivation by these transcription factors (By similarity). Heterodimer of an alpha and a beta subunit. Interacts with HIVEP3 (By similarity). The alpha subunit binds DNA as a monomer and through the Runt domain. DNA-binding is increased by heterodimerization. Interacts with XRCC6 (Ku70) and XRCC5 (Ku80). Interacts with MYST3 and MYST4.

Subunit:
Heterodimer of an alpha and a beta subunit. Interacts with HIVEP3. The alpha subunit binds DNA as a monomer and through the Runt domain. DNA-binding is increased by heterodimerization. Interacts with G22P1 (Ku70) and XRCC5 (Ku80). Interacts with MYST3 and MYST4.

Subcellular Location:
Nucleus.

Tissue Specificity:
Specifically expressed in osteoblasts.

Post-translational modifications:
Phosphorylated; probably by MAP kinases (MAPK). Isoform 3 is phosphorylated on Ser340.

DISEASE:
Defects in RUNX2 are the cause of cleidocranial dysplasia (CLCD) [MIM:119600]; also known as cleidocranial dysostosis (CCD). CLCD is an autosomal dominant skeletal disorder with high penetrance and variable expressivity. It is due to defective endochondral and intramembranous bone formation. Typical features include hypoplasia/aplasia of clavicles, patent fontanelles, wormian bones (additional cranial plates caused by abnormal ossification of the calvaria), supernumerary teeth, short stature, and other skeletal changes. In some cases defects in RUNX2 are exclusively associated with dental anomalies.

Similarity:
Contains 1 Runt domain.

SWISS:
Q13950

Gene ID:
860

Database links:

Entrez Gene: 860 Human

Entrez Gene: 12393 Mouse

Entrez Gene: 100155806 Pig

Entrez Gene: 367218 Rat

Omim: 600211 Human

SwissProt: Q13950 Human

SwissProt: Q9XSB7 Horse

SwissProt: Q08775 Mouse

SwissProt: Q9Z2J9 Rat

Unigene: 535845 Human

Unigene: 391013 Mouse

Unigene: 391017 Mouse

Unigene: 214214 Rat

Unigene: 83672 Rat

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

RUNX2又称：Cbfα1(Core-binding factor, alpha 3 subunit) 是新发现的一类调控间充质干细胞向成骨方向分化的特异性转录因子,参与骨形成,骨骼生长和发育的一类重要细胞,它起源于多能间充质干细胞,是间充质干细胞在体内的各种调控因素的调节下发育而成的。