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Merck
CN

ABE1953

Anti-PTRF/Cavin-1 Antibody

from rabbit, purified by affinity chromatography

别名:

Polymerase I and transcript release factor, PTRF/Cavin-1, Cavin-1

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
polyclonal
Application:
ICC, IHC, WB
Citations:
1
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biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

rat, human

technique(s)

immunocytochemistry: suitable, immunohistochemistry: suitable (paraffin), western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... CAVIN1(284119)

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General description

Polymerase I and transcript release factor (UniProt Q6NZI2; also known as Cavin-1, PTRF, RNA polymerase I and transcript release factor, TTF-I interacting peptide 12) is encoded by the PTRF (also known as CGL4, CAVIN, CAVIN1, FKSG13) gene (Gene ID 284119) in human. Cavin-1 is the founding member of the PTRF/Cavin family of cytoplasmic proteins whose expressions are essential for caveola formation. PTRF/Cavin-1, serum deprivation response (SDR)/Cavin-2, SDR-related gene product that binds to C kinase (SRBC)/Cavin-3, and muscle-restricted coiled-coil protein (MURC)/Cavin-4, form an oligomeric assembly termed Cavin complex in the cytosol and associate with caveolin at plasma membrane caveolae. Research shows an essential role for PTRF/Cavin-1 but not the other family members in caveola formation and recruitment of the cavin complex to the plasma membrane. In prostate cancer PC3 cells and during development of zebrafish notochord, lack of PTRF-Cavin expression correlates with lack of caveolae, where caveolin displays increased lateral mobility on the plasma membrane and accelerated lysosomal degradation. Expression of Cavin-1 restores caveolae formation in PC3 cells. Likewise the absence of cavin-1 is also observed in advanced prostate carcinoma. PTRF gene mutations are known to cause congenital generalized lipodystrophy 4 (CGL4).
~52 kDa observed.

Immunogen

Linear peptide corresponding to the N-terminus of human PTRF/Cavin-1.

Application

Anti-PTRF/Cavin-1 Antibody is an antibody against PTRF/Cavin-1 for use in Western Blotting, Immunohistochemistry (Paraffin), Immunocytochemistry.
Western Blotting Analysis: A representative lot detected PTRF/Cavin-1 expression in HeLa, but not in prostate cancer cell lines, LNCaP, 22Rv1 and PC-3 (Moon, H., et al. (2014). Oncogene 33(27):3561-3570).
Western Blotting Analysis: A representative lot detected exogenously expressed human PTRF/Cavin-1 in transfected 22Rv1 and LNCaP cells (Moon, H., et al. (2014). Oncogene 33(27):3561-3570).
Immunohistochemistry Analysis: A representative lot detected reduced PTRF/Cavin-1 immunoreactivity in paraffin-embedded malignant prostate stroma tissue samples when compared with normal prostate stroma and benign prostatic hyperplasia (BPH) specimens. A lack of PTRF/cavin-1 immunoreactivity in prostate epithelia was seen among both normal and malignant samples (Moon, H., et al. (2014). Oncogene 33(27):3561-3570).
Immunocytochemistry Analysis: A representative lot detected surface caveola localization of exogenously expressed human PTRF/Cavin-1 among transfected LNCaP cells (Moon, H., et al. (2014). Oncogene 33(27):3561-3570).

Biochem/physiol Actions

Expected to react with spliced isoforms 1 and 2, but not isoform 3.

Analysis Note

Evaluated by Western Blotting in rat skeletal muscle myoblast L6 cell lysate.

Western Blotting Analysis: A 1:1,000 dilution of this antibody detected PTRF/Cavin-1 in 10 µg of rat skeletal muscle myoblast L6 cell lysate.

Other Notes

Concentration: Please refer to lot specific datasheet.

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存储类别

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Bayader Annabi et al.
International journal of stem cells, 10(1), 103-113 (2016-12-28)
Tumour necrosis factor (TNF)-α activation of mesenchymal stromal cells (MSC) enhances their tumour-suppressive properties and tumour-homing ability. The molecular actors involved are unknown. We found that TNF induced MSC migration and tubulogenesis which correlated with a dose-dependent increase in Cavin-1

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