추천 제품
생물학적 소스
mouse
Quality Level
항체 형태
purified antibody
항체 생산 유형
primary antibodies
클론
8-5-2, monoclonal
종 반응성
mouse, sheep, human, rat, bovine
제조업체/상표
Upstate®
기술
western blot: suitable
동형
IgG
NCBI 수납 번호
UniProt 수납 번호
배송 상태
wet ice
타겟 번역 후 변형
phosphorylation (pTyr694/pTyr699)
유전자 정보
human ... STAT5A(6776)
일반 설명
STAT (Signal Transducers and Activators of Transcription) are a family of conserved transcription factors that transduce high-fidelity signals for the cytokine family of ligands and receptors as the principle substrates of JAK kinases (1,2). In resting cells, the STATs exist in an inactive state in the cytoplasm until activated. Activators include cytokines, growth factors, and some peptides. These activate JAK kinases, which when activated, bind to the STAT SH2 (Src homology domain-2) domain resulting in phosphorylation of STAT (1). Upon activation, STAT1, -3, -4, -5A, and -5B all form homodimers. STAT1 and STAT2, as well as STAT1 and STAT3 form heterodimers, and several STATs form tetramers, depending on the variables of the activating ligand (1). After dimerization, the STATs accumulate in the nucleus by way of nuclear transport (1). STAT5A and STAT5B appear to be most important to the function of growth hormone and prolactin and play critical roles in milk production (1,2,3). The phosphorylation of Tyrosine 694/699 is a hallmark of activated STAT5.
특이성
Specific for the phosphorylated tyrosine residue 694 of STAT5A (94kDa) and 699 of STAT5B (92kDa). Unidentified proteins may be detected in some lysates.
면역원
Epitope: Tyr694/699
KLH-conjugated, synthetic phosphopeptide (KAVDG[pY]VKPQIK) corresponding to amino acids 689-700 of STAT5A and 694-705 of STAT5B. Clone 8-5-2.
애플리케이션
Anti-phospho-STAT5A/B (Tyr694/699) Antibody, clone 8-5-2 is a mouse monoclonal antibody for detection of phospho-STAT5A/B (Tyr694/699) also known as signal transducer & activator of transcription 5A/B & has been validated in WB.
품질
Routinely evaluated by Western Blot on 3T3/A31 cells stimulated with PDGF or HeLa cells stimulated with interferon-α.
Western Blot Analysis: 0.5-2 μg/mL of this lot detected phosphorylated STAT5A/B in lysates from 3T3/NIH cells stimulated with PDGF. 0.5-2 μg/mL of a previous lot detected phosphorylated STAT5A/B in lysates from 3T3/A31 cells stimulated with PDGF and from HeLa cells stimulated with interferon-a (IFN-a).
Western Blot Analysis: 0.5-2 μg/mL of this lot detected phosphorylated STAT5A/B in lysates from 3T3/NIH cells stimulated with PDGF. 0.5-2 μg/mL of a previous lot detected phosphorylated STAT5A/B in lysates from 3T3/A31 cells stimulated with PDGF and from HeLa cells stimulated with interferon-a (IFN-a).
표적 설명
STAT5A (94 kDa) and STAT5B (92 kDa)
물리적 형태
Format: Purified
Purified mouse monoclonal IgG in buffer containing PBS. Frozen solution at -20°C.
분석 메모
Control
IFN-α induced HeLa cells or GM-CSF treated TF-1 cells
IFN-α induced HeLa cells or GM-CSF treated TF-1 cells
기타 정보
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
법적 정보
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
Leptin enhances STAT-3 phosphorylation in HC11 cell line: effect on cell differentiation and cell viability.
Molecular and cellular endocrinology null
A mutant Stat5b with weaker DNA binding affinity defines a key defective pathway in nonobese diabetic mice.
The Journal of Biological Chemistry null
Increased sensitivity to GH in liver of Ames dwarf (Prop1df/Prop1df) mice related to diminished CIS abundance.
The Journal of Endocrinology null
Up-regulation of SLAP in FLI-1-transformed erythroblasts interferes with EpoR signaling.
Blood null
American journal of physiology. Endocrinology and metabolism, 292(6), E1856-E1862 (2007-03-01)
Gram-negative sepsis with release of endotoxin is a frequent cause of cachexia that develops partly because of resistance to growth hormone (GH) with reduced insulin-like growth factor-I (IGF-I) expression. We set out to more fully characterize the mechanisms for the
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