HSD17B1 Antibody [C12F18] | Primary Antibodies

Application: Reactivity: Human

Lane 1: 293T, Lane 2: 293T (human HSD17B1 transfected)

Usage Information

Dilution
WB1:10000 - 1:50000 IP1:50 IHC1:100 - 1:250 FCM1:250

Application
WB, IP, IHC, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

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
35 kDa 35 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 placenta tissue; JEG3 cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
HSD17B1 Antibody [C12F18] detects endogenous levels of total HSD17B1 protein.

Clone
C12F18

Synonym(s)
E17KSR; EDH17B1; EDH17B2; EDHB17; SDR28C1; HSD17B1; 17-beta-hydroxysteroid dehydrogenase type 1; 17-beta-HSD 1; 20 alpha-hydroxysteroid dehydrogenase; E2DH; Estradiol 17-beta-dehydrogenase 1; Placental 17-beta-hydroxysteroid dehydrogenase; Short chain dehydrogenase/reductase family 28C member 1; 20-alpha-HSD

Background
HSD17B1, or 17β-hydroxysteroid dehydrogenase 1, functions as a short-chain dehydrogenase/reductase enzyme critically converting inactive estrone (E1) to potent estradiol (E2) in estrogen-dependent tissues like ovary granulosa cells, endometrium, and breast, featuring a 328-residue homodimeric structure (~34.5 kDa/subunit) with an N-terminal Rossmann fold (αβα sandwich) housing the NADPH cofactor-binding site via a positively charged Arg37 salt bridge to the 2'-phosphate, a catalytic triad of Ser142-Tyr155-Lys159 proton-relaying a hydride from NADPH's pro-R face to C17-keto of E1 (or androstenedione to testosterone) through a conserved Tyr155 hydrogen bond polarizing the carbonyl, and a narrow hydrophobic C-terminal substrate tunnel accommodating steroid orientation with His221 enabling substrate inhibition at high E1 levels by reverse non-productive binding. This NADPH-preferred reduction (over NAD+) amplifies local E2 for ERα binding driving proliferation via cyclin D1/CCND1 upregulation and anti-apoptosis through Bcl-2, fueling estrogen receptor-positive breast cancer growth (overexpressed in 30-50% of cases correlating with poor tamoxifen response), endometrial hyperplasia/carcinoma via paracrine E2 excess, endometriosis lesion expansion from ectopic HSD17B1, and prognostic HSD17B1/HSD17B2 imbalance; inhibitors like letrozole derivatives or ebselen target the catalytic triad to suppress intratumoral E2 without systemic hypoestrogenism.

Background

HSD17B1, or 17β-hydroxysteroid dehydrogenase 1, functions as a short-chain dehydrogenase/reductase enzyme critically converting inactive estrone (E1) to potent estradiol (E2) in estrogen-dependent tissues like ovary granulosa cells, endometrium, and breast, featuring a 328-residue homodimeric structure (~34.5 kDa/subunit) with an N-terminal Rossmann fold (αβα sandwich) housing the NADPH cofactor-binding site via a positively charged Arg37 salt bridge to the 2'-phosphate, a catalytic triad of Ser142-Tyr155-Lys159 proton-relaying a hydride from NADPH's pro-R face to C17-keto of E1 (or androstenedione to testosterone) through a conserved Tyr155 hydrogen bond polarizing the carbonyl, and a narrow hydrophobic C-terminal substrate tunnel accommodating steroid orientation with His221 enabling substrate inhibition at high E1 levels by reverse non-productive binding. This NADPH-preferred reduction (over NAD+) amplifies local E2 for ERα binding driving proliferation via cyclin D1/CCND1 upregulation and anti-apoptosis through Bcl-2, fueling estrogen receptor-positive breast cancer growth (overexpressed in 30-50% of cases correlating with poor tamoxifen response), endometrial hyperplasia/carcinoma via paracrine E2 excess, endometriosis lesion expansion from ectopic HSD17B1, and prognostic HSD17B1/HSD17B2 imbalance; inhibitors like letrozole derivatives or ebselen target the catalytic triad to suppress intratumoral E2 without systemic hypoestrogenism.

References
https://pubmed.ncbi.nlm.nih.gov/27102893/ https://pubmed.ncbi.nlm.nih.gov/28430630/

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

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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%