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Anti-NDRG1 Rabbit Antibody [P3F2]

Catalog No.: F3886

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:10000 - 1:50000 IP1:10 - 1:100 IHC1:250 - 1:500 IF1:100 - 1:250

Application
WB, IP, IHC, IF

Reactivity
Mouse, Rat, Human

Source
Rabbit

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
43 kDa 43 kDa, 48 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human colon; Human normal kidney; Human liver; Mouse colon; Rat colon; Mouse brain; Rat brain; HEK-293T; HeLa; LNCaP; Rat-1 (starved for 4 h, insulin, 20nM); C2C12 (insulin, 20nM)
Negative Control

Datasheet & SDS

Biological Description

Specificity
NDRG1 (P3F2) Rabbit mAb detects endogenous levels of total NDRG1 protein.

Clone
P3F2

Synonym(s)
CAP43, DRG1, RTP, NDRG1, Protein NDRG1, Differentiation-related gene 1 protein, N-myc downstream-regulated gene 1 protein, Nickel-specific induction protein Cap43, Reducing agents and tunicamycin-responsive protein, Rit42, DRG-1

Background
NDRG1, originally identified as a reducing agent and tunicamycin-responsive protein (RTP), is located on human chromosome 8q24.3. It is transcribed as a 3.0 kb mRNA containing a 1182 bp open reading frame, which encodes a 394–amino acid protein with a molecular weight of approximately 43 kDa. NDRG1 is primarily localized in the cytoplasm but can also associate with the plasma membrane and nucleus. Functionally, it participates in a wide range of cellular processes, including embryonic development, differentiation, maintenance of genomic stability, metabolism, apoptosis, and autophagy. As a stress-responsive gene, NDRG1 expression is induced by multiple stimuli such as chemical agents, metal ions, DNA damage, endoplasmic reticulum stress, and hypoxia. In cancer biology, NDRG1 displays context-dependent roles. In many malignancies—including oral, esophageal, gastric, colon, liver, lung, and bladder cancers—NDRG1 is upregulated and acts in an oncogenic capacity. Its major oncogenic role involves promoting cell motility, thereby enhancing invasion, migration, and angiogenesis. Additional tumor-promoting functions include supporting tumor initiation and stemness, accelerating cell growth, and contributing to resistance against radio- and chemotherapy. Conversely, NDRG1 also exhibits tumor-suppressive properties. It is downregulated in cancers such as prostate, renal, pancreatic, and endometrial tumors, as well as in neuroblastoma. NDRG1 has been reported to inhibit cell motility, suppress tumor initiation and stemness, and trigger apoptosis. NDRG1 functions as a multifunctional regulator of cancer progression, with dual roles as either an oncogene or a tumor suppressor. Its effect appears to be highly dependent on tissue type and the specific cellular environment, reflecting its complex role in modulating malignant transformation.

Background

NDRG1, originally identified as a reducing agent and tunicamycin-responsive protein (RTP), is located on human chromosome 8q24.3. It is transcribed as a 3.0 kb mRNA containing a 1182 bp open reading frame, which encodes a 394–amino acid protein with a molecular weight of approximately 43 kDa. NDRG1 is primarily localized in the cytoplasm but can also associate with the plasma membrane and nucleus. Functionally, it participates in a wide range of cellular processes, including embryonic development, differentiation, maintenance of genomic stability, metabolism, apoptosis, and autophagy. As a stress-responsive gene, NDRG1 expression is induced by multiple stimuli such as chemical agents, metal ions, DNA damage, endoplasmic reticulum stress, and hypoxia. In cancer biology, NDRG1 displays context-dependent roles. In many malignancies—including oral, esophageal, gastric, colon, liver, lung, and bladder cancers—NDRG1 is upregulated and acts in an oncogenic capacity. Its major oncogenic role involves promoting cell motility, thereby enhancing invasion, migration, and angiogenesis. Additional tumor-promoting functions include supporting tumor initiation and stemness, accelerating cell growth, and contributing to resistance against radio- and chemotherapy. Conversely, NDRG1 also exhibits tumor-suppressive properties. It is downregulated in cancers such as prostate, renal, pancreatic, and endometrial tumors, as well as in neuroblastoma. NDRG1 has been reported to inhibit cell motility, suppress tumor initiation and stemness, and trigger apoptosis. NDRG1 functions as a multifunctional regulator of cancer progression, with dual roles as either an oncogene or a tumor suppressor. Its effect appears to be highly dependent on tissue type and the specific cellular environment, reflecting its complex role in modulating malignant transformation.

References
https://pubmed.ncbi.nlm.nih.gov/35563887/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3
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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%