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AB6000

Sigma-Aldrich

Anti-TIMP-3 Antibody, CT

from rabbit, purified by affinity chromatography

Synonym(s):

MIG-5, TIMP metallopeptidase inhibitor 3, Tissue inhibitor of metalloproteinases 3

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

horse, human, rat

species reactivity (predicted by homology)

pig (based on 100% sequence homology), primate (based on 100% sequence homology), equine (based on 100% sequence homology), canine (based on 100% sequence homology), monkey (based on 100% sequence homology), mouse (95% homology), bovine (based on 100% sequence homology)

technique(s)

immunocytochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... TIMP3(7078)

General description

Tissue inhibitor of metalloproteinases 3 (TIMP-3) is a member of the TIMP family. The TIMPs are so named because they are slow, tight binding endogenous inhibitors of the Matrix Metalloproteinases (MMPs). The four TIMPs have different inhibition constants for the different MMPs studied. TIMPs have been shown to have activity against the ADAMs family of proteinases. TIMP-3 is an efficient "sheddase" inhibitor, inhibiting ADAM-17 (TACE) at the low nanomolar levels seen with MMP inhibition. The other ADAMs proteinases have not yet been assayed for TIMP inhibition, but TIMP-2 seems to be much less active on ADAM-17 than isTIMP-3. TIMP-3 is thought to be constitutively produced by many cell types and is inducible in others. The TIMP-3 localization differs from the other 3 TIMPs, and is thought to be primarily deposited into the extracellular matrix.

Specificity

The antibody recognizes TIMP-3 at the C-terminus. Does not appear to cross react with TIMP-1 or TIMP-2.

Immunogen

Epitope: C-terminus
KLH-conjugated linear peptide corresponding to human TIMP-3 at the C-terminus.

Application

Immunocytochemistry Analysis: 1:500 dilution from a previous lot detected TIMP-3 in C6 cells.
Research Category
Cell Structure
Research Sub Category
MMPs & TIMPs
This Anti-TIMP-3 Antibody, C-terminus is validated for use in WB, IC for the detection of TIMP-3.

Quality

Evaluated by Western Blot using an HL-60 cell lysate supplemented with PMA-conditioned media.

Western Blot Analysis: 0.5 µg/ml of this antibody detected TIMP-3 on 10 µg of HL-60 in PMA-conditioned media.

Target description

Bands may be observed for reduced protein bands at ~ 24 kDa (unglycosylated) and ~ 30 kDa (glycosylated). Additional TIMP-3 bands MAY be visible at 50 kDa (dimer), 12 kDa, and 15 kDa (breakdown products) and sample dependent.

Linkage

Replaces: AB802

Physical form

Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Analysis Note

Control
HL-60 cell lysate in PMA-conditioned media.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Ioannis Kanakis et al.
Arthritis & rheumatology (Hoboken, N.J.), 71(4), 571-582 (2018-11-01)
Cartilage destruction in osteoarthritis (OA) is mediated mainly by matrix metalloproteinases (MMPs) and ADAMTS. The therapeutic candidature of targeting aggrecanases has not yet been defined in joints in which spontaneous OA arises from genetic susceptibility, as in the case of
Qitao Zhang et al.
Experimental eye research, 178, 212-222 (2018-10-20)
The daily shedding and renewal of photoreceptor outer segments (OS) is critical for maintaining vision. This process relies on the efficient uptake, degradation, and sorting of shed OS material by the retinal pigment epithelium (RPE). Poor OS degradation has been
Jung Hyun Park et al.
Journal of personalized medicine, 12(5) (2022-05-29)
Tissue inhibitor of metalloproteinase-3 (TIMP-3) is a component of the extracellular environment and is suggested to play an indirect role in regulating Aβ production and the pathophysiology of Aβ deposition in brains. However, studies on the amount of TIMP-3 in
Sarah Naessens et al.
Human mutation, 40(5), 539-551 (2019-01-23)
Sorsby fundus dystrophy (SFD) is a macular degeneration caused by mutations in TIMP3, the majority of which introduce a novel cysteine. However, the exact molecular mechanisms underlying SFD remain unknown. We aimed to provide novel insights into the functional consequences
Anna Paola Carreca et al.
International journal of molecular sciences, 22(5) (2021-03-07)
Ectodomain shedding is a key mechanism of several biological processes, including cell-communication. Disintegrin and metalloproteinases (ADAMs), together with the membrane-type matrix metalloproteinases, play a pivotal role in shedding transmembrane proteins. Aberrant shedding is associated to several pathological conditions, including arthritis.

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