SLURP1 Antibody, FITC conjugated

Code CSB-PA021784LC01HU
Size US$166
Order now
Have Questions? Leave a Message or Start an on-line Chat

Product Details

Full Product Name
Rabbit anti-Homo sapiens (Human) SLURP1 Polyclonal antibody
Uniprot No.
Target Names
SLURP1
Alternative Names
SLURP1 antibody; ARS antibody; Secreted Ly-6/uPAR-related protein 1 antibody; SLURP-1 antibody; ARS component B antibody; ARS(component B)-81/S antibody; Anti-neoplastic urinary protein antibody; ANUP antibody
Raised in
Rabbit
Species Reactivity
Human
Immunogen
Recombinant Human Secreted Ly-6/uPAR-related protein 1 protein (23-103AA)
Immunogen Species
Homo sapiens (Human)
Conjugate
FITC
Clonality
Polyclonal
Isotype
IgG
Purification Method
>95%, Protein G purified
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, PH 7.4
Form
Liquid
Troubleshooting and FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time
Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

Customer Reviews and Q&A

 Customer Reviews

There are currently no reviews for this product.

Submit a Review here

Target Background

Function
Has an antitumor activity. Was found to be a marker of late differentiation of the skin. Implicated in maintaining the physiological and structural integrity of the keratinocyte layers of the skin. In vitro down-regulates keratinocyte proliferation; the function may involve the proposed role as modulator of nicotinic acetylcholine receptors (nAChRs) activity. In vitro inhibits alpha-7-dependent nAChR currents in an allosteric manner. In T cells may be involved in regulation of intracellular Ca(2+) signaling. Seems to have an immunomodulatory function in the cornea. The function may implicate a possible role as a scavenger receptor for PLAU thereby blocking PLAU-dependent functions of PLAUR such as in cell migration and proliferation.
Gene References into Functions
  1. These findings strongly suggest that down regulation of SLURP1 expression may be implicated in the pathogenesis of various solid tumors, particularly malignancies of squamous lineage, and thus this gene may be a squamous lineage-specific tumor suppressor. PMID: 29231248
  2. This is the first mal de Meleda case of Javanese ethnicity to be documented, and the unique mutation has not previously been reported. PMID: 29023701
  3. We identified a mutation in SLURP1 in five members of a consanguineous family in Pakistan, who had Mal de Meleda. PMID: 29226984
  4. novel splice site mutation c.58+5G>T in mal de Meleda in India PMID: 26254200
  5. Results of this study suggest understand Mal de Meleda, it will be important to identify proteins that interact with mutatated SLURP1. In any such studies, it will be important to assess binding of mutant SLURP1 proteins that cause Mal de Meleda. PMID: 25919322
  6. To our knowledge, the present study is the fi rst report on molecular investigation of Mal de Meleda from Libya. PMID: 24738704
  7. This supports the hypothesis that the antiproliferative activity of SLURP-1 is related to 'metabotropic' signaling pathway through alpha7-nAChR, that activates intracellular signaling cascades without opening the receptor channel. PMID: 26905431
  8. SLURP1 participates in pathophysiology of psoriasis by regulating keratinocyte proliferation and differentiation, and by suppressing the growth of S. aureus PMID: 26474319
  9. Palmoplantar keratoderma of the Gamborg-Nielsen type is caused by mutations in the SLURP1 gene and represents a variant of Mal de Meleda. PMID: 24604124
  10. rSLURP-1 decreased production of TNFalpha by T-cells, downregulated IL-1 beta and IL-6 secretion by macrophages, and moderately upregulated IL-10 production by both types of immunocytes PMID: 24877120
  11. This report further expands the spectrum of clinical phenotypes associated with mutations in SLURP1 in the Mediterranean population. PMID: 24093092
  12. mutations in SLURP1 as a cause for mal de Meleda and suggest an ancient founder effect for p.W15R in the western European population. PMID: 23290002
  13. Those findings suggested that SLURP-1 and stimulus through alpha7 nicotinic ACh receptors actively controlled asthmatic condition by stimulating ciliary beating and also by suppressing airway inflammation. PMID: 23876317
  14. The pro-oncogenic effects of tobacco nitrosamine (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) can be abolished, in part, by rSLURP-1 that also upregulated RUNX3. PMID: 22369755
  15. Patients with Mal de Meleda with the homozygous SLURP-1 G86R mutation may have an impaired T-cell activation PMID: 20854438
  16. Results indicate that activation of alpha(7)-nAChR by SLURP-1 leads to upregulation of NF-kappaB gene expression due to activation of the Raf-1/MEK1/ERK1/2 cascade that proceeds via two complementary signaling pathways. PMID: 20660165
  17. These findings suggest that SLURP-1 may play an important role in the control and maintenance of the periodontal ligament by protecting the periodontal ligament fibroblasts from apoptosis. PMID: 20337899
  18. Those findings suggest that diminished expression of SLURP-1 in asthma attenuates its negative regulation of airway inflammation, and that perhaps changes in SLURP-1 expression could serve as a marker of airway damage in asthma. PMID: 20621062
  19. Our findings indicate that the MDM type of transgressive PPK is caused by SLURP-1 mutations in patients from various origins and demonstrate allelic heterogeneity for mutations in SLURP-1. PMID: 12483299
  20. Novel mutations in the gene encoding protein-SLURP-1 and 5 haplotypes in Mal de Meleda. Founder mutation, conserved cysteine residue to tyrosine (C99Y), in inbred pedigree, and a signal sequence mutation (W15R), homozygous and heterozygous. PMID: 12603845
  21. Recurrent nonsense mutation, R96X, in four families of Turkish descent. These families share common ancestral haplotype at mal de Meleda locus, suggesting founder effect. PMID: 12787122
  22. Identification of SLURP1 as an epidermal neurotransmitter explains the clinical phenotype of Mal de Meleda. PMID: 14506129
  23. ARS Component B and its protein product SLURP1 are implicated in maintaining the physiological and structural integrity of the keratinocyte layers of the skin. PMID: 14721776
  24. Mutation analysis revealed a homozygous missense mutation (G86R) in exon 3 of ARS gene of this patient PMID: 15909066
  25. Biological role of SLURP-1 in the epidermis is to provide fine tuning of the physiologic regulation of keratinocyt functions through the cholinergic pathways. PMID: 16354194
  26. anti-tumorigenic activities of SLURP-1 and -2 were demonstrated both in vitro and in vivo. PMID: 17643396
  27. SLURP-1 participates in the regulation of gut immune functions and motility, as well as possibly playing a role in colon carcinogenesis/cancer progression. PMID: 18764860
  28. these results expand the spectrum of mutations in SLURP-1 gene. PMID: 19692209

Show More

Hide All

Involvement in disease
Mal de Meleda (MDM)
Subcellular Location
Secreted.
Tissue Specificity
Granulocytes. Expressed in skin. Predominantly expressed in the granular layer of skin, notably the acrosyringium. Identified in several biological fluids such as sweat, saliva, tears, plasma and urine.
Database Links

HGNC: 18746

OMIM: 248300

KEGG: hsa:57152

STRING: 9606.ENSP00000246515

UniGene: Hs.103505

icon of phone
Call us
301-363-4651 (Available 9 a.m. to 5 p.m. CST from Monday to Friday)
icon of address
Address
7505 Fannin St., Ste 610, Room 7 (CUBIO Innovation Center), Houston, TX 77054, USA
icon of social media
Join us with

Subscribe newsletter

Leave a message

* To protect against spam, please pass the CAPTCHA test below.
CAPTCHA verification
© 2007-2024 CUSABIO TECHNOLOGY LLC All rights reserved. 鄂ICP备15011166号-1
webinars: DT3C facilitates antibody internalization X
Place an order now

I. Product details

*
*
*
*

II. Contact details

*
*

III. Ship To

*
*
*
*
*
*
*

IV. Bill To

*
*
*
*
*
*
*
*