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Documentos clave

I3536

Sigma-Aldrich

Insulina human

recombinant, expressed in yeast, γ-irradiated, suitable for cell culture

Sinónimos:

Insulin human

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About This Item

Fórmula empírica (notación de Hill):
C257H383N65O77S6
Número de CAS:
Peso molecular:
5807.57
MDL number:
UNSPSC Code:
12352209
NACRES:
NA.77
biological source:
Saccharomyces cerevisiae
form:
lyophilized powder

biological source

Saccharomyces cerevisiae

Quality Level

recombinant

expressed in yeast

sterility

γ-irradiated

form

lyophilized powder

potency

≥25 USP units per mg

technique(s)

cell culture | mammalian: suitable

solubility

0.01 M HCl: 20 mg/mL, clear, colorless to faintly yellow

UniProt accession no.

shipped in

ambient

storage temp.

−20°C

InChI key

PBGKTOXHQIOBKM-FHFVDXKLSA-N

Gene Information

human ... INS(3630)

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General description

The INS gene encodes for preproinsulin, which is enzymatically converted into insulin. Insulin is produced in the insulin-producing pancreatic β cells. Preproinsulin is converted to proinsulin in ER and proinsulin is then proteolytically processed to form insulin in newly-forming insulin secretory granules. Insulin production is tightly regulated by specific DNA elements present within ∼400 bp in the proximal region of the INS promoter.

Application

Insulin human has been used for the following applications:
  • For adipogenic differentiation assays (in the preparation of medium supplement)
  • Incubation of cells for the evaluation of the effects of insulin
  • Mass spectrometry (used for the external caliberation)

Biochem/physiol Actions

Hormona polipeptídica bicatenaria producida por las células β de los islotes pancreáticos. Su peso molecular es de ~ 5800 Da) Las cadenas α y β se unen por dos enlaces disulfuro intercatenarios. La cadena α contiene un puente disulfuro intracatenario. La insulina regula la captación, utilización y almacenamiento celulares de glucosa, aminoácidos y ácidos grasos, e inhibe la hidrólisis de glucógeno, proteínas y grasas.
Regula la captación, utilización y almacenamiento celulares de glucosa, aminoácidos y ácidos grasos, e inhibe la hidrólisis de glucógeno, proteínas y grasas.
Insulin is responsible for two types of actions- excitatory and inhibitory. In its excitatory role, it increases the uptake of glucose and lipid synthesis, and in its inhibitory role it inhibits glycogenolysis, gluconeogenesis, lipolysis, proteolysis and ketogenesis. Aberrant insulin secretion leads to various disorders such as diabetes, hyperglycemia or hypoglycaemia. Type I diabetes is a result of autoimmune destruction of β cells of pancreas, which leads to depletion of insulin. Mutant INS-gene Induced Diabetes of Youth (MIDY) syndrome is an autosomal dominant disorder caused by missense mutations, which lead to aberrant proinsulin folding. Impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) is caused by resistance to insulin-stimulated glucose uptake.

Other Notes

InChI: 1S/C257H383N65O77S6/c1-29-131(23)205(313-193(339)104-259)252(393)317-204(130(21)22)248(389)288-159(75-82-200(349)350)217(358)282-156(71-78-189(263)335)221(362)308-183-116-403-404-117-184-243(384)305-178(111-324)240(381)294-162(88-123(7)8)225(366)295-168(95-140-53-61-146(329)62-54-140)228(369)283-154(69-76-187(261)333)218(359)290-161(87-122(5)6)223(364)285-158(74-81-199(347)348)220(361)302-174(101-190(264)336)235(376)298-170(97-142-57-65-148(331)66-58-142)231(372)309-182(242(383)304-176(255(396)397)103-192(266)338)115-402-401-114-181(214(355)273-107-194(340)278-153(72-79-197(343)344)216(357)281-151(51-42-84-271-257(267)268)212(353)272-108-195(341)279-166(93-138-46-36-32-37-47-138)227(368)297-167(94-139-48-38-33-39-49-139)230(371)299-171(98-143-59-67-149(332)68-60-143)238(379)320-208(135(27)327)254(395)322-85-43-52-186(322)246(387)286-152(50-40-41-83-258)222(363)321-209(136(28)328)256(398)399)311-250(391)203(129(19)20)316-236(377)164(90-125(11)12)292-229(370)169(96-141-55-63-147(330)64-56-141)296-224(365)160(86-121(3)4)289-210(351)133(25)277-215(356)157(73-80-198(345)346)287-247(388)202(128(17)18)315-237(378)165(91-126(13)14)293-233(374)173(100-145-106-270-120-276-145)301-239(380)177(110-323)280-196(342)109-274-213(354)180(113-400-405-118-185(310-244(183)385)245(386)319-207(134(26)326)253(394)306-179(112-325)241(382)318-206(132(24)30-2)251(392)312-184)307-226(367)163(89-124(9)10)291-232(373)172(99-144-105-269-119-275-144)300-219(360)155(70-77-188(262)334)284-234(375)175(102-191(265)337)303-249(390)201(127(15)16)314-211(352)150(260)92-137-44-34-31-35-45-137/h31-39,44-49,53-68,105-106,119-136,150-186,201-209,323-332H,29-30,40-43,50-52,69-104,107-118,258-260H2,1-28H3,(H2,261,333)(H2,262,334)(H2,263,335)(H2,264,336)(H2,265,337)(H2,266,338)(H,269,275)(H,270,276)(H,272,353)(H,273,355)(H,274,354)(H,277,356)(H,278,340)(H,279,341)(H,280,342)(H,281,357)(H,282,358)(H,283,369)(H,284,375)(H,285,364)(H,286,387)(H,287,388)(H,288,389)(H,289,351)(H,290,359)(H,291,373)(H,292,370)(H,293,374)(H,294,381)(H,295,366)(H,296,365)(H,297,368)(H,298,376)(H,299,371)(H,300,360)(H,301,380)(H,302,361)(H,303,390)(H,304,383)(H,305,384)(H,306,394)(H,307,367)(H,308,362)(H,309,372)(H,310,385)(H,311,391)(H,312,392)(H,313,339)(H,314,352)(H,315,378)(H,316,377)(H,317,393)(H,318,382)(H,319,386)(H,320,379)(H,321,363)(H,343,344)(H,345,346)(H,347,348)(H,349,350)(H,396,397)(H,398,399)(H4,267,268,271)/t131-,132-,133-,134+,135+,136+,150-,151-,152-,153-,154-,155-,156-,157-,158-,159-,160-,161-,162-,163-,164-,165-,166-,167-,168-,169-,170-,171-,172-,173-,174-,175-,176-,177-,178-,179-,180-,181-,182-,183-,184-,185-,186-,201-,202-,203-,204-,205-,206-,207-,208-,209-/m0/s1

Storage Class

13 - Non Combustible Solids

wgk_germany

WGK 2

flash_point_c

Not applicable


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Y Nakamura et al.
British journal of pharmacology, 123(4), 675-682 (1998-03-28)
1. The actions of troglitazone, pioglitazone, metformin and bezafibrate, agents that improve insulin-resistance, on voltage-dependent Ca2+ channels in arterial smooth muscle cells were examined by use of the conventional and nystatin-perforated whole-cell clamp methods. Single cells were freshly isolated from
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G M Reaven
Diabetes, 37(12), 1595-1607 (1988-12-01)
Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose

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